
COPYRIGHT DEPOSm 



INTERNAL MEDICINE 



BY 

DAVID BOVAIRD, Jr., A.B., M.D. 

ASSISTANT PROFESSOR OF CLINICAL MEDICINE IN THE COLLEGE OF PHYSICIANS 
AND SURGEONS OF COLUMBIA UNIVERSITY ; ASSOCIATE VISITING PHYSICIAN ^ 
OF THE PRESBYTERIAN HOSPITAL, AND VISITING PHYSICIAN OF O 
THE SEASIDE HOSPITAL, IN THE CITY OF NEW YORK 



WITH 109 ILLUSTRATIONS IN THE TEXT AND 
7 COLORED PLATES 




PHILADELPHIA & LONDON 

J. B. LIPPINCOTT COMPANY 



Copyright, 1912 
By J. B. LipPiNCOTT Company 



Printed by J. B. Lippincott Company 
The Washington Square Press, Philadelphia, U. 



To 



HENRY FAIRFIELD OSBORN, LLD., D.Sc. 

PROFESSOR OF ZOOLOGY IN COLUMBIA 
UNIVERSITY, AND FORMERLY PROFESSOR OF 
COMPARATIVE ANATOMY IN PRINCETON 
UNIVERSITY, THIS BOOK IS DEDICATED IN 
GRATEFUL RECOGNITION OF THE FACT THAT 
FROM HIM THE WRITER FIRST LEARNED 
THE JOY OF INDEPENDENT STUDY AND 
INVESTIGATION 



PREFACE 



Doubtless there has rarely been a teacher of medicine who has been 
satisfied with the books which his students have had to use. The large 
treatises are too long, too rich in information for those entering upon 
the study of medicine, while many of the shorter works are mere cata- 
logues of facts. It has seemed to the writer, after many years ' teaching, 
that there was a distinct need both among students and practitioners of 
a work which should give in compact form the more important facts of 
the subjects included in the domain of internal medicine. Just as the 
modern builder rears his frame-work of steel and upon this suspends 
the walls, the floors and the ornamentation of his building, so the student 
must outline his subject in his mind, and later add the details. The 
beauty of the building will depend upon the finish, its strength must lie 
in the frame-work. The purpose of the present work is to supply the 
frame-work of internal medicine. 

The title has been chosen in recognition of the need of a term which 
shall denote those subjects left of the older " practice of medicine " 
when all the specialties have been subtracted from it, those subjects which 
are, after all, the fundamentals of our study. 

The arrangement of the subjects has been dictated by the wish to put 
the simpler first, and to present something of a logical order of study. 
The placing of some subjects, such as that of small-pox, among diseases 
due to animal parasites, is questionable, but in such instances it has seemed 
well to follow the best leading we have at present, although we may he 
uncertain of its correctness. The final classification of many of the 
familiar diseases must long remain doubtful. Syphilis has for years 
been regarded as surely a bacterial disease and classified accordingly. 
The recent studies apparently prove the specific organism to belong to 
the lower orders of the animal kingdom. At any time further investi- 
gation may restore the disease to its older position. In like manner the 
specific agents of scarlet fever, measles, and other exanthemata are as- 
sumed to be bacteria, and these diseases are placed accordingly. The 
eager investigations now going on in so many laboratories may any day 
give one or more of these diseases a new position. We must act upon 
our present knowledge, with full consciousness that much of it may to- 
morrow require revision. 

The lack of ilbistration in the current works on our subject has been 
very striking in this day when photography is so readily available and 
is so great an aid in the presentation of any subject. It has been a source 
of pleasure that the publishers have wished to make full use of this aid 

V 



vi 



PREFACE 



and have so heartily assisted the author in his efforts to this end. To 
the many friends who have loaned their treasures to him, the author 
renews his thanks. The effort has been made to render due recognition 
for such assistance. 

Especial thanks are due to my friends, Dr. Walter B. James for aid in 
writing the chapter on Cardiac Arrhythmia, and Dr. Lewis A. Conner for 
much valuable aid in the preparation of the text. 

The Author. 

New York, August, 1912. 



CONTENTS 



I 

DISEASES or THE RESPIRATORY TRACT 

PAGE 



Diseases of the Nose 1 

Acute Rhinitis 1 

Autumnal Catarrh 2 

Epistaxis 3 

Diseases of the Laryxx 3 

Acute Laryngitis 3 

Chronic Laryngitis 4 

Edematous Laryngitis 4 

Tuberculous Laryngitis 5 

Syphilitic Laryngitis G 

Xeuroses of the Larynx 7 

Diseases of the Broxchi 7 

Acute Bronchitis 7 

Chronic Bronchitis 9 

Fibrinous Bronchitis 10 

Bronchiectasis 10 

Bronchial Asthma 12 

Bronchopulmonary Hemorrhage 14 

Diseases of the Lungs 15 

Disturbance of Circulation 15 

Acute Congestion 15 

Passive Congestion 15 

Edema of the Lungs 16 

Embolism, Thrombosis and Infarction 16 

Atelectasis : 17 

Lobar Pneumonia 18 

Bronchopneumonia 28 

Chronic Interstitial Pneumonia 32 

Pneumonoconiosis 33 

Emphysema 35 

Atrophic Emphysema 37 

Acute Vesicular Emphysema 37 

Interstitial Emphysema 37 

Abscess of the Lung 37 

Gangrene of the Lung 40 

New Growths of the Lung 41 

Diseases of the Pleura 42 

Acute Pleurisy 42 

Fibrinous Pleurisy 43 

Serous Pleurisy 43 

Purulent Pleurisy 50 

Special Forms of Pleurisy 52 

Chronic Pleurisy 53 

Hydrothorax 54 

Pneumothorax, Hydropneumothorax, Pyopneumothorax 54 

II 

DISEASES OF THE DIGESTIVE SYSTEM 

Diseases of the Mouth 57 

Stomatitis 57 

Catarrhal Stomatitis 57 

Herpetic or Aphthotis Stomatitis 57 



vii 



viii CONTENTS 

I PAGB 

Ulcerative Stomatitis 57 

Parasitic Stomatitis 58 

Gan<irenoiis Stomatitis 58 

Acute and Chronic Glossitis 59 

Geographical Tongue 59 

Leukoplakia Buccalis 59 

Diseases of the Salivary Glaxds 59. 

Disturbance of Secretion 59 

Acute Parotitis 59 

Chronic Parotitis 60 

Von Mikulicz's Disease GO 

Diseases of the Pharynx GO 

Acute Catarrhal Pharyngitis 60 

Chronic Pharyngitis GO 

Retropharyngeal Abscess 60 

Diseases of the Toxsils 61 

Acute Follicular Tonsillitis 61 

Suppurative Tonsillitis 62. 

Hypertrophy of Tonsils and Adenoid Vegetations 62 

Diseases of the Esophagus 63 

Acute Esophagitis 63 

Ulceration of the Esophagus 63 

Spasm of the Esophagus 63 

Stenosis of the Esophagus 64 

Cancer of the Esophagus 65 

Diverticulum of the Esophagus 65 

Dilatation of the Esophagus 65 

Diseases of the Stomach " 65 

Acute Gastritis 65 

Toxic Gastritis 66 

Phlegmonous Gastritis 67 

Chronic Gastritis 67 

Ulcer of the Stomach 69 

Cancer of the Stomach = 73 

Acute Dilatation of the Stomach 76 

Chronic Dilatation of the Stomach 77 

Congenital Hypertrophic Stenosis of the Pylorus 79 

Hemorrhage from the Stomach 80 

Neuroses of the Stomach 81 

Sensory Neuroses 81 

Secretory Neuroses 82 

Motor Neuroses 82 

Diseases of the Intestines 83 

Enteritis 83 

Croupous Enteritis 85 

Phlegmonous Enteritis 85 

Cholera Nostras 85 

Diarrheal Diseases of Childhood 86 

Acute Intestinal Indigestion 86 

Acute Gastro-Enteric Infection 87 

lleo-Colitis 87 

Intestinal Ulcers 89 

ClioU'ra 90 

Dysentery 93 

Acute Catarrhal Dysentery 93 

Acule Specilie Dysentery 94 

Amchic Dysentery 94 

Diphtlieritic Dysentery 95 

Chronic Dysentery 9(5 

Ap]iendi('itia 96 

Intestinal Ohst ruet ion 102 



CONTENTS ix 

PAGE 

Constipation 107 

Enteroptosis 109 

Neuroses of the Intestine... 110 

Mucous Colitis 112 

Cancer of the Intestine 113 

Diseases of the Liver 115 

Jaundice 115 

Obstructive Jaundice 115 

Toxemic Jaundice ; 116 

Acute Yellow Atrophy of the Liver 116 

Disturbances of the Hepatic Circulation 118 

Diseases of the Blood-Vessels of the Liver 119 

Embolism or Thrombosis 119 

Suppurative Pylephlebitis 119 

Cirrhoses of the Liver 120 

Biliary Cirrhosis 124 

Absces's of the Liver 125 

New Growths of the Liver 127 

Fatty Liver 129 

Amyloid Liver 129 

Anomalies in Form and Position of Liver 130 

Diseases of the Bile-Passages and Gall-Bladder 131 

Acute Catarrh of the Bile-Duets 131 

Chronic Catarrhal Angiocholitis 131 

Suppurative and Ulcerative Angiocholitis 132 

Acute Infectious Cholecystitis 132 

Cholelithiasis 133 

Diseases of the Pancreas 137 

Acute Hemorrhagic Pancreatitis 137 

Suppurative Pancreatitis 138 

Chronic Pancreatitis 139 

Pancreatic Cyst 140 

Carcinoma of the Pancreas 140 

Pancreatic Calculi 141 

Diseases of the Peritoneum 142 

Acute General Peritonitis 142 

Localized Peritonitis 144 

Chronic Peritonitis 146 

New Growths of the Peritoneum 147 

Ascites 147 

III 

DISEASES OF THE KIDNEYS 

Anomalies of Form and Position 150 

Movable Kidney 151 

Congestion of the Kidney 152 

Anomalies of Secretion 152 

Anuria 152 

Hematuria 152 

Hemoglobinuria 153 

Albuminuria 153 

Pyuria 154 

Chyluria 154 

Lithuria 154 

Oxaluria 155 

Cystinuria 155 

Plio>i)haturia 155 

Indicanuria 15G 

Uremia 150 

Functional Efficiency of the Kidneys 158 

Acute Nephritis 160 



X CONTENTS 

PAGE 

Chronic Nephritis 162 

Chronic Parenchymatous Nephritis 163 

Chronic Interstitial Nephritis 165 

Amyloid Disease of the Kidney 168 

Cystic Disease of the Kidney 169 

Pyelitis 170 

Nephrolithiasis 171 

Hydronepluosis 173 

Perinephritic Absfcss 173 . 

Tumors of tlie Kidney 174 

IV 

DISEASES OF THE CIRCULATORY SYSTEM 

Diseases of the Pericardium 175 

Pericarditis 175 

Chronic Adhesive Pericarditis 181 

Tuberculous Pericarditis 182 

Other Affections of the Pericardium 182 

Diseases of the Heart 183 

Endocarditis 183 

Acute Endocarditis 183 

Malignant and Septicemic Endocarditis 185 

Chronic Endocarditis 187 

Chronic Valvular Heart Disease 188 

Mitral Insufficiency 193 

Mitral Stenosis. . ."^ 194 

Aortic Insufficiency 195 

Aortic Stenosis 198 

Pulmonary Insufficiency. 199 

Pulmonary Stenosis 199 

Tricuspid Insuffioieiicy „ 200 

Tricuspid Stenosis 201 

Combined Valvular Lesions of the Heart 201 

Hypertrophy of the Heart 208 

Hypertrophy of the Left Ventricle , 209 

Dilatation of the Heart 209 

Diseases of the Myocardium 211 

]Myocarditis 211 

Acute Myocarditis 212 

Chronic Myocarditis 213 

Fatty Heart 213 

Neuroses of the Heart 214 

Palpitation 214 

Tachycardia (Rapid Heart) 215 

Bradycardia (Slow Heart) 216 

Arrhytliniia 216 

Angina I'cetoris 226 

Toxic Angina 227 

Congenital Defects of the Heart 228 

Diseases of the Arteries : 229 

Acute Aortitis 229 

Arteriosclerosis 229 

Aneurism 232 

Aneurism of Ascending Portion of the Arch 234 

Aneurism of the Transverse Arch 235 

Aneurism of Descending Part of Arch 236 

Aneurism of Thoracic and Abdominal Aorta 236 

Diseases of the Veins 239 

Acute Phlebitis 239 

Tlironibosis. 242 

1 Icmorrlioids 243 



CONTENTS xi 

V 

DISEASES OF THE BLOOD AND DUCTLESS GLANDS 

PAGE 

Anemia 246 

Chlorosis 246 

Secondary Anemia 247 

Pernicions Anemia 248 

Leukemia , 249 

Splenomyelogenous Leukemia 250 

Lymphatic Leukemia 250 

Pseudoleukemia 253 

Purpura 255 

Hemophilia .• . . 257 

Morbus ]\Iaculosus Neonatorum 259 

Scurvy 259 

Infantile Scurvy 260 

Status Lymphaticus 262 

Diseases of the Suprarenal Bodies 262 

Addison's Disease 262 

Diseases of the Spleex 263 

Movable Spleen 263 

Rupture of Spleen 264 

infarct and Abscess of Spleen 264 

Tumors of Spleen 264 

Splenomegaly 264 

Polycythemia 266 

Diseases of the Thyroid Gland 267 

Congestion 267 

Acute Thvroiditis 267 

Goitre . . 267 

Tumors of the Tliyroid 268 

Exophthalmic Goitre 268 

Myxedema 271 

Cretinism 272 

Myxedema 272 

Diseases of the Thymus Gland 274 

VI 

CONSTITUTIONAL DISEASES 

Chronic Polyarthritis 276 

Muscular Pvheumatism 279 

Gout 280 

Diabetes Mellitus 284 

Diabetes Insipidus 289 

Rachitis 290 

Achondroplasia 293 

Obesity 294 

VII 

INTOXICATIONS AND ^MISCELLANEOUS DISEASES 

Alcoholism > 296 

Opium: Poisoning 299 

Morphine Habit 299 

Cocaine Poisoning 301 

Cocaine Habit 301 

Chronic Lead Poisoning 301 



xii 



CONTENTS 



Chronic Arsenic Poisoning 303 

Food Poisoning 304 

Carbon Monoxide Poisoning 307 

Sunstroke 308 

Diseases of the :Muscles 309 

Myositis 309 

Myotonia Congenita 310 

Myasthenia Gravis 311 

Paraniyocloniis Multiplex 311 

Rare Diseases of the Bones and Joints 312 

VIII 

THE INFECTIOUS DISEASES 

Typhoid Fever 313 

Typhus Fever 332 

Relapsing Fever 335 

Influenza (La Grippe) 337 

Dengue 339 

Yellow Fever 339 

Plague 342 

Malta Fever 344 

Beri-beri 345 

Scarlet Fever 346 

Measles ! 352 

Rubella (German Measles) (Rotlieln) 355 

Diphtheria 355 

Diphtheroid Inflammations 368 

Whooping-Cough 369 

Mumps 371 

Septicemia 374 

Pyemia 376 

Erysipelas 377 

Acute Rheumatic Fever 379 

Gonorrheal Infection 383 

Ti i!i:!:( i i.osLS 385 

Lki'kosv 414 

Tetanus 416 

Infectious Diseases of Doubtful Nature 417 

Febrieula 417 

Weil's Disease 418 

Miliary Fever 419 

C;iaiulular Fever 419 

.Milk Sickness 419 

Rocky Mountain Spotted Fever 420 

Pellagra 420 

Infkci lors Diseases Common to Man and Lower Animals 421 

ClaiKlcrs 421 

llv(ln.i)li()hiii 423 

Ant li rax 425 

Act iiK. mycosis 426 

Diseases Cai skd by X'kgetable Parasites (^theu titan Bacteria 427 



CONTENTS xiii 
IX 

DISEASES CAUSED BY ANIMAL PARASITES 

PAGE 

Protozoan Diseases 429 

Malaria 429 

Syphilis 441 

Small-pox 451 

Vaccination 457 

Varicella 458 

Trypanosomiasis 459 

Kala-azar 461 

Other Parasitic Protozoa 462 

Diseases Due to Animal Parasites Other than Protozoa-Met azo a 462 

Diseases Caused by Trematodes 462 

Distomatosis 462 

Diseases Caused by Nematodes 464 

Ascariasis 464 

Oxyuriasis 465 

Trichiniasis 466 

Uncinariasis 469 

Filariasis 471 

Dracontiasis 474 

Diseases Caused by Cestodes 475 

Intestinal Infections 475 

Tenia-Mediocanellata 475 

Tenia Solium 476 

Dibothriocephalus Latus 476 

Hymenolepis Nana 476 

Visceral Infections 479 

Cysticercus Cellulosae 479 

Ecliinococcus Disease 479 

X 

DISEASES OF THE NERVOUS SYSTEM 

Diseases of the Nerves 482 

Neuritis . 482 

Neuromata 484 

Diseases of the Cerebral Nerves 485 

Olfactory Nerve and Tract 485 

Optic Nerve and Tract 486 

Oculomotor Nerve 488 

Fourth Nerve 488 

Sixth Nerve (Nerve Abducens") 488 

Fifth or Trigeminus Nerve 489 

Facial Nerve 490 

Auditory Nerve 491 

Glosso-pharyngeal Nerve 492 

Pneumogastric (Vagus) Nerve 493 

Spinal Accessory Nerve 494 

Hypoglossal Nerve 495 

Diseases of the Spinal Nerves 496 

Cervical Plexus 406 

Brachial Plexus 497 

Lumbar Plexus 498 

Sacral Plexus 498 

Sciatica 498 

Diseases of the Spinal Cord and ^Meninges 499 

Spinal Pachynicniiigitis 49!) 

Spinal Leptonioniiigil is 500 

Afiections of the lilood-X'csscls and Circulation of the Cord 501 

Caisson Disease 502 

Myelitis 50;) 



xiv CONTENTS 

PAGE 

Compression of the Spinal Cord 505 

Acute Poliomyelitis 50G 

Acute Ascending Paralysis 508 

Progressive Muscular Atrophy 509 

Glosso-labio-laryngeal Paralysis 511 

The Spinal Scleroses 512 

Locomotor Ataxia 512 

Lateral Sclerosis 515 

Hereditary Spastic Spinal Paralysis 516 

Ataxic Paraplegia (Gowers) 517 

Hereditary Ataxia or Friedreich's Ataxia 517 

Syringomyelia 518 

Tumors of the Spinal Cord 522 

Diseases of the Brain and Meninges 523 

Diseases of the Meninges 523 

Pachymeningitis 523 

Leptomeningitis 524 

Cerebrospinal Meningitis 524 

Tuberculous Meningitis 525 

Acute Suppurative Meningitis 525 

Afl'ections of the Blood-Vessels and Circulation of the Brain 531 

Thrombosis of Cerebral Sinuses and Veins 531 

Cerebral Anemia 531 

Cerebral Hyperemia , 531 

Cerebral Edema 532 

Cerebral Hemorrhage, Embolism and Thrombosis 532 

Cerebral Paralysis of Childhood 537 

Hydrocephalus 538 

Abscess of the Brain 539 

General Paresis 540 

Multiple Sclerosis 543 

Tumors and Cysts of the Brain 544 

Aphasia 547 

Amaurotic Family Idiocy 549 

Functional Nervous Diseases 549 

Acute Delirium 549 

Paralysis Agitans 550 

Acute Chorea 551 

Convulsions of Children 553 

Epilepsy 555 

Migraine 558 

Neuralgia 559 

Tetany 562 

Occupation Neuroses 564 

Hysteria 565 

Neurasthenia 570 

Traumatic Neuroses 575 

Functional Paralyses 576 

Periodical Paralysis 576 

Astasia-Abasia 577 

Vasomotor and Trophic Disorders 577 

Raynaud's Disease 577 

Erythromelalgia 578 

Facial Hemiatrophy 579 

Angioneurotic Edema 579 

Scleroderma 580 

Acromegaly 580 

APPENDIX 

General Care of the Sick 582 

Standard Diets 592 

Taiu-k of Equivalent Weights and Measures 596 



LIST OF ILLUSTRATIONS 

PA.GE 



1. "Clubbed fingers" of a patient having broncliiectasis 11 

2. Temperature in lobar pneumonia 21 

3. Temperature in lobar pneumonia, short course 22 

4. Temperature in bronchopneumonia 30 

5. Radiogram of siderosis of the lung 34 

6. Radiogram of an abscess of the lung 39 

7. Radiogram of a new growth of the lung 41 

8. Temperature in pleurisy with effusion 44 

9. Line of dulness in pleurisy with effusion 45 

10. Pleural effusion with Grocco's triangle 46 

11. The Potain aspirator 48 

12. Aspiration of the chest 49 

13. Empyema presenting externally empyema necessitatis 51 

14. Pyopneumothorax 56 

15. Radiogram of an esophagus dilated from stricture 64 

16. Bleeding ulcer of the stomach 71 

17. Perforating ulcer of the stomach 72 

18. Hypertrophic stenosis of the pylorus 79 

19. Intussusception 103 

20. Radiogram of a displaced stomach, gastroptosis 110 

21. Radiogram of a displaced colon Ill 

22. Process of natural cure in cirrhosis of the liver 123 

23. An ascitic abdomen 148 

24. Horse-shoe kidney 150 

25. Large white kidney 164 

26. Small contracted kidney, surface 166 

27. Small contracted kidney, section 166 

28. Cystic kidney 169 

29. Cystic kidney 169 

30. Temperature curve of perinephritic abscess 174 

31. Heart covered by plastic pericardial effusion 176 

32. Area of dulness of pericardial effusion and the obtuse cardiohepatic angle. . 178 

33. Outlines of cardiac dulness at successive stages of pericardial effusion. . . . 179 

34. Temperature curve in septicemic endocarditis 186 

35. A diagrammatic representation of the heart 189 

36. Janeway sphygmomanometer 207 

37. Auriculo-ventricular bundle 217 

38. Ulcer of the septum involving the a. -v. bundle 218 

39. Pulse tracings 219 

40. Electrocardiogram of healthy adult male 222 

41. Electrocardiogram in auricular fibrillation 225 

42. Aneurism of the arch of the aorta 234 

43. Edema of face and arms caused by pressure of an aneurism 236 

44. Radiogram of an aortic aneurism 237 

45. Dilatation of superficial veins of chest and abdomen following occlusion 

of superior vena cava 240 

46. Outline of spleen in splenomyclogenous leukemia 251 

XV 



xvi LIST OF ILLUSTRATIONS 

PAGB 

47. Enlarged cervical and axillary lymph-nodes of Hodgkin's disease 254 

48. An extensive purpura of the legs 256 

49. Outlines of liver and spleen in splenic anemia 265 

50. Polycythemia with cyanosis 266 

51. Graves' disease 269 

52. Graves' disease 270 

53. Cretin, front view 272 

54. Cretin, back view 272 

55. Myxedema, face 273 

56. Myxedema, hands 273 

57. Chronic polyarthritis 277 

58. Arthritis deformans 278 

59. Diabetic gangrene 286 

60. Achondroplasia 292 

61. Temperature curve of typhoid fever 320 

62. Temperature curve of typhoid fever 321 

63. Typhoid fever eruption 323 

64. Temperature curve in relapsing fever 336 

65. Temperature curve in influenza 338 

66. Stegomyia fasciata 341 

67. Temperature curve in scarlet fever 348 

68. Scarlet fever desquamation 349 

69. Temperature curve in measles 353 

70. Preparation of patient for nasal irrigation or intubation 362 

71. Nasal irrigation in diphtheria 363 

72. Intubation instruments 365 

73. Intubation in upright position 366 

74. Intubation in supine position 367 

75. Mumps 372 

76. Temperature curve in septicopyemia 375 

77. Temperature curve in erysipelas 378 

78. Temperature curve in chronic pulmonary tuberculosis 399 

79. Radiogram of tuberculosis of the left apex 404 

80. Pellagra 421 

81. Glanders eruption 422 

82. Protozoa. 430 

83. Malaria, tertian fever 435 

84. Malaria, quotidian fever 436 

85. Gumma of the knee 444 

86. Congenital syphilis 446 

87. Small-pox, the facial eruption 453 

88. Small-pox, a late stage of the eruption 454 

89. Bilharzia hematobia 463 

90. Ascaris lumbricoides 465 

91. Ovum of ascaris Ininbricoides 465 

92. Oxyuris verniuiilaris 466 

93. Facies in trichiniasis 467 

94. Temperature curve of trichinosis 468 

95. Uneinaria ' 470 

96. Ovum of uneinaria 471 

97. Ovum of Ankylastomum duodenale in feces 472 

98. Filaria Bancrofti in blood 473 



LIST OF ILLUSTRATIONS xvii 

PAGE 

99. Tenia mediocanellata 476 

100. Tenia solium 477 

101. Hymenolepis nana 478 

102. Ovum of hymenolepis nana 478 

103. The optic chiasm 486 

104. Atrophy in syringomyelia, front view 519 

105. Atrophy in syringomyelia, back view 520 

106. Contralateral reflex in meningitis 527 

107. Identical reflex in meningitis 527 

108. Eruption of cerebrospinal meningitis 528 

109. Herpes zoster 561 

COLORED PLATES 

PLATE I. Lesions of the Mouth 57 ' 

PLATE II. KoPLiK's Spots 35S ; 

PLATE III. The Eruptions of Measles and Scarlet Fever 353 

PLATE IV. Negri Bodies 423 

PLATE V. Malarial Parasites, Tertian and Quartan 432 

PLATE VI. Malarial Parasites, Estivo- Autumnal .433> 

PLATE VII. The Fundus in Amaurotic Family Idiocy 549 ■■ 

0 



Internal Medicine 



I. 

DISEASES OF THE RESPIRATORY TRACT 

DISEASES OF THE NOSE 

ACUTE RHINITIS 

(Acute Coryza. Acute Nasal Catarrh) 

Definition. — An acute inflammation of the nasal mucous membrane. 

Etiology. — The affection is common at all ages, especially during the 
winter and spring months. Exposure to cold and wet is the most 
frequent antecedent. The various bacteria to be found in the nose are 
believed to have a part in the causation. The affection is frequently 
transmitted from one member of a household to the others and may 
become epidemic. An acute rhinitis belongs to the invasion of measles. 

Morbid Anatomy. — The nasal mucous membrane is congested and 
swollen, sometimes to such a degree as to block the nares; it is dry at 
the beginning, later covered by a free secretion of mucus or muco-pus. 

Symptoms. — These are general and local. (1) General: There is 
usually more or less malaise, muscular soreness or pains in various 
parts of the body, wdth or without fever. The temperature may rise 
to 100° or 102°, and the pulse be quickened correspondingly. (2) Local: 
Sneezing may mark the onset. The nose becomes dry and uncomfort- 
able, and in the course of a few hours the nares are obstructed by the 
swelling and a free mucous secretion is established. This secretion 
often irritates the nares and upper lip, causing an eczema. Usually 
there is headache and, if the tear ducts are involved, lachrymation. After 
two or three days the swelling subsides, the secretion becomes thicker and 
muco-purulent, and the inflammation disappears in a week or two. The 
constitutional symptoms regularly vanish with the acute condition. 
The senses of smell and taste are often markedly impaired for some time 
after an attack. 

Complications. — Acute coryza is often only part of a general in- 
flammation of the nose, throat, and bronchi, or the process beginning 
in the nose extends to the lower parts of the respiratorv^ tract. Otitis 
media from extension through the naso-pharynx and Eustachian tubes 
is not uncommon. At times the process extends into the antrum or 
the frontal sinuses with resulting severe local symptoms. 

1 



2 



DISEASES OF THE RESPIRATORY TRACT 



Treatment. — Rest in bed is best for all severe cases, and is essential 
for children and the aged. Free diaphoresis and evacuation of the 
bowels are desirable at the onset. A hot bath, followed by hot tea or 
lemonade, with Dover's powder, 10 grains, or 5 to 10 grains of aspirin, 
will usually cause free sweating. As a laxative two or three grains of 
calomel may be given at night, with a Seidlitz powder or other saline in 
the morning. Locally a mild antiseptic spray, such as Dobell's solution, 
either full strength or diluted to one-half strength, should be used every 
two or three hours. If there is much obstruction adrenalin chloride 
1/2000-1/5000 will usually give relief. Later astringent applications, 
such as argyrol (20 per cent.) or nitrate of silver, will serve to reduce the 
inflammation and check the secretion. The influence of internal medi- 
cation is doubtful, but small doses of Dover's powder, or combinations of 
camphor, extract of belladonna, and quinine are commonly given. 

AUTUMNAL CATARRH 
(Hay Fever) 

Definition. — An inflammation of the nasal mucous membrane, due 
to the action of the pollen of certain plants and grasses, and frequently 
associated ^Yith. asthma. 

Etiology. — The disease appears to have its basis in a hypersensitive 
condition of the nasal mucous membrane peculiar to certain individuals. 
This susceptibility is marked in some families and is frequently inherited. 
The young and middle-aged suffer most often, and the tendency seems 
to diminish in old age. 

The active excitant is regularly the pollen of certain plants and 
grasses. Dunbar has found that the pollen of many plants and grasses 
may be active. Different pollens are concerned in the production of 
the spring and autumnal catarrhs. For the spring hay-fever of the 
United States the pollen of grasses and sedges seems most effective, 
though a number of plants also produce active pollen. In the autumn 
the spring and autumnal catarrhs. For the spring hay fever of the 
agent. It has been found that the poisonous principle in these pollens 
is a toxalbumin, which can be readily extracted. 

Symptoms. — The disease appears about the first of May or in the 
autumnal type in August. The onset is marked by sneezing, which 
is quickly followed by lachrymation and a profuse watery coryza. The 
nasal mucous membrane becomes swollen and the nares are blocked. 
There is more or less tickling, itching, or pain in the eyes, nose, and 
throat. The patients are depressed and languid. Temperature and 
pulse are normal. Asthma may develop at any time. These sjonptoms 
persist for about six weeks and then clear up. The attacks are repeated 
yearly at the same time. 

Treatment. — Attacks may be avoided by going to sea, or hy residence 
in places where the vegetation is scant. Various mountain resorts are 
popular. Dunbar has perfected a serum from which he claims good 
results. The serum must be given daily throughout the hay-fever season. 



DISEASES OF THE LARYNX 



3 



As a palliative a nasal spray of adrenalin chloride 1 to 2000 to 1 to 
5000 may be serviceable. Many patients have been improved or cured 
by the removal of hypertrophied turbinates, or nasal spurs, or adequate 
treatment of other pathological conditions of the nose. 

EPISTAXIS 

Bleeding from the nose is a symptom rather than a disease in itself. 
The causes are either local or constitutional. The local include (1) 
trauma of any kind, picking the nose, violent sneezing or coughing, and 
the like; (2) the presence of foreign bodies; (3) neoplasms, which are 
, very rare. The general include (1) a tendency present in growing 
children, especially the delicate and rheumatic; (2) the onset of acute 
infections, especially typhoid fever; (3) abnormal conditions of the 
blood, such as hemophilia, purpura, scurvy, pernicious anemia, or 
leukemia; (4) chronic nephritis and cirrhosis of the liver; (5) vicarious 
menstruation; (6) the changes of pressure induced by ascending moun- 
tains. 

Symptoms. — The blood flows from one or both nostrils. If the 
patient is lying down the blood may be swallowed and later vomited, 
or it may be coughed up. In most cases there are no other symptoms. 
If the loss of blood is excessive, the patient becomes weak and syncope 
may occur. Death from nasal hemorrhage is very rare except in cases 
of hemophilia. 

Treatment. — In most cases the hemorrhage ceases spontaneously. 
The application of ice to the nose or snuffing up ice-water will hasten 
the cessation. The head should be held up. Plugging the anterior nares 
with absorbent cotton is usually all that is necessary. In severer cases 
a spray of adrenahn chloride 1 to 2000 to 1 to 5000 may suffice. If not^ 
both anterior and posterior nares should be firmly packed with gauze. 
Packing the posterior nares may be done by means of a catheter through 
the tip of which a silk thread is passed into the pharynx and thence 
drawn out of the mouth for the attachment of the post-nasal pad of 
gauze. Belocq's canula, if available, renders this procedure much easier. 
Such packing may be kept in place for not more than 48 hours. The 
danger of infection in these cases is great, and asepsis should be practised 
as far as possible. Calcium lactate may be given, 20 to 30 grains 
thrice daily, and injections of serum, as for hemophilia (see page 257), 
resorted to if other measures fail. 

DISEASES OF THE LARYNX 

ACUTE LARYNGITIS 

This affection is frequently part of a general catarrh of the respira- 
tory tract. It may occur alone, either as an independent or as a 
secondary process. 

Etiology. — It is caused by exposure to cold, the inhalation of 
irritating gases, the swallowing of corrosive liquids, or excessive speak- 



4 DISEASES OF THE RESPIRATORY TRACT 



ing. It occurs in measles and influenza and other acute infectious 
diseases as part of the catarrhal inflammation of the respiratory tract. 
Acute rhinitis or pharyngitis frequently involves the lar^^nx by ex- 
tension. 

Symptoms. — Discomfort on swallowing, hoarseness, a croupy cough, 
and rarely aphonia. The temperature is usually but little raised and 
the constitutional symptoms are slight. In children acute laryngitis is 
often associated with severe dyspnea, as in spasmodic croup. In adults 
edema of the larynx may occur, but is rare. Laryngeal examination 
shows congestion and swelling of the vocal cords and the adjacent parts 
of the larynx. 

Course. — The affection regularly subsides in a few days or at most 
a week. An acute bronchitis frequently follows from the do\mward 
extension of the process. 

Treatment. — Rest for the larynx is important. The milder cases 
often require no other treatment. Various simple lozenges may be given 
for the patient's comfort. Children and adults Avith severe symptoms 
should be put to bed, and the air of the room kept warm and moist. 
Inhalations of steam impregnated with the compound tincture of benzoin 
(oi to the pint of boiling water) should be given for fifteen minutes 
three or four times a day. Cold applications or an ice-bag to the throat 
may help. Children with dyspnea should be treated as for spasmodic 
croup. 

CHRONIC LARYNGITIS 

Etiology. — Repeated attacks of acute laryngitis, persistent over-use 
of the voice, the constant inhalation of dust or tobacco smoke, may be 
the cause. Nasal obstruction often plays an important part. 

Symptoms. — The voice is hoarse, and there is a hoarse cough. Pain 
or constitutional disturbances are usually lacking. On examination the 
vocal cords are slightly congested, lustreless, and possibly thickened, 
and there is some swelling and congestion of the aryepiglottic folds. 

Diagnosis. — Care must be taken to exclude other forms of chronic 
laryngitis, especially the tuberculous and syphilitic. (See pp. 5 and 6.) 

Treatment. — The cause, if known, must be removed. Nasal ob- 
struction, if present, must be relieved. For the laryngitis itself, rest 
and astringent applications either by brush or spray of 3 per cent, nitrate 
of silver, 3 per cent, perchloride of zinc, or 10 per cent, argyrol may be. 
employed. The general condition of the patient must be imp>roved by all 
possible means. A mild, equable climate with an atmosphere free from 
dust is favorable. 

EDEMATOUS LARYNGITIS 
(Edema of the Glottis) 

Etiology. — This very serious affection is met with as a complication 
(1) of either acute or chronic laryngitis; (2) of severe inflammation 
of the throat, such as diphtheria, or of the neck, such as erysipelas or 



DISEASES OF THE LARYNX 



5 



cellulitis; (3) of acute infectious diseases, such as typhoid, typhus or 
scarlet fever; (4) acute or chronic Bright 's disease; (5) angioneurotic 
edema. 

Symptoms. — The picture is that of sudden, rapid strangulation, with 
rapidly increasing dyspnea, hoarseness, stridor, cyanosis, and, unless 
relief is secured, death from cardiac failure. On laryngoscopic examina- 
tion an enormous boggy swelling of the epiglottis, the aryepiglottic folds 
and adjacent parts may be seen. In some cases the swelling of the 
epiglottis may be seen on direct inspection and may be felt by the 
finger. 

Treatment. — Cracked ice should be given by mouth and also applied 
externally; spraying the throat with cocaine, 4 per cent, or better, 
adrenalin chloride 1 to 2000, may give relief. If not, the edematous 
parts may be scarified. Finally intubation or tracheotomy may be 
required. 

TUBERCULOUS LARYNGITIS 

Etiology. — The disease is rarely primary in the larynx. Almost 
invariably examination of the lungs will reveal a focus at one or both 
apices. 

Morbid Anatomy. — Beginning as an anemia or hyperemia, the dis- 
ease soon shows its characteristic tubercles in and upon the epiglottis, 
aryepiglottic folds, and the interarytenoid tissues. The tubercles later 
break down, leaving broad ulcers. The disease may extend and involve 
the pharynx or esophagus. In some cases the ulceration is deep and the 
cartilages of the larynx are destroyed. 

Symptoms. — (1) The disease begins with slight hoarseness, which 
gradually increases to complete aphonia. (2) Cough and expectoration 
develop later. The cough may be paroxysmal and exceedingly trouble- 
some. (3) Dysphagia occurs in the more advanced eases and may be 
intense. If the epiglottis is destroyed every attempt to swallow produces 
great pain and choking. (4) The patients regularly show the fever, 
emaciation, and other symptoms, of pulmonary tuberculosis. 

Laryngoscopic examination in the early stages shows only an anemia 
with thickening due to infiltration of the laryngeal mucous membrane, 
especially that over the aryepiglottic folds. Later all the structures 
about the glottis become greatly thickened, and broad, shallow ulcers, 
with gray bases and ill-defined edges, appear. In the final stages the 
epiglottis may be destroyed, and the ulcers extend into the pharynx 
or esophagus. The lungs give the physical signs of pulmonary tuber- 
culosis and the sputum shows the bacilli, but not always on the first 
examination. 

Treatment. — These cases must for the most part be treated as cases 
of pulmonary tuberculosis. Locally inhalations of compound tincture 
of benzoin may give relief in the early stages. Later applications of 
lactic acid in glycerin, 5 per cent, at first, increasing gradually to 50 
per cent., are advocated. Intratracheal injections of menthol, 1 per cent. 



6 



DISEASES OF THE RESPIRATORY TRACT 



in olive oil, 1 to 3 drams at each sitting, may be given. For the relief of 
distress anesthesin may be used as a powder or as a 5 per cent, suspension 
in oil. In the final stages coeain or morphine may be required. 

SYPHILITIC LARYNGITIS 

The larynx may be involved in either the secondary or tertiary 
stage of syphilis. 

Symptoms. — Hoarseness first calls attention to the larynx, later the 
voice may be lost. Some cough and expectoration are present, and 
in the severer forms dysphagia. Edema of the glottis may occur in 
severe cases. Examination of the larynx shows in the secondary stage a 
congestion indistinguishable from simple laryngitis, or superficial ulcera- 
tion Avhich may be extensive. Mucous patches or condylomata are rare. 
In the tertiary stage gummata may be seen, especially at the base of 
the epiglottis, or deep ulcers when the gummata break down. Later 
extensive cicatrization which may, cause stenosis of the larynx results. 
The laryngeal lesions of inherited syphilis are of like character, gummata, 
ulcers, and cicatrization. 

Diagnosis. — The diagnosis of syphilis can usually be safely made 
from the history and the associated symptoms in the skin, glands, and 
throat. The Wassermann reaction should be tried and if ulcers are 
present the spirochete may be sought. 

Treatment. — The constitutional treatment of syphilis must be thor- 
oughly carried out. The tertiarj^ lesions are always refractory to treat- 
ment. Tracheotomy may be required. 

NEUROSES OF THE LARYNX 

Two forms of spasm of the larynx are recognized and described as 
Laryngismus Stridulus and Spasmodic Croup. 

1. Laryngismus Stridulus. — This affection is peculiar to infants 
from six months to two years of age, especially the rachitic. It is 
characterized by recurrent attacks of spasm of the adductor muscles 
of the larynx. These attacks are often excited by reproof or punishment, 
and are spoken of as passion fits" or attacks of " holding the breath." 
The affection is thought by some to be closely related to the attacks of 
dyspnea associated with enlargement of the thymus, the so-called thymic 
asthma; by others it is considered a manifestation of tetany. 

Symptoms. — The attacks occur either by day or night. The child 
suddenly stops breathing, becomes cyanotic, and looks as though about 
to die, or in some cases struggles for breath, which, the spasm relaxing, 
is finally drawn in with a long stridulous cry, the so-called ''crow." 
Convulsions may occur with the attack. The attacks recur frequently 
in some cases. In rare instances death occurs. 

Treatment. — The underlying rachitis must be appropriately treated, 
by fresh air, good food, and sunshine. Daily cold sponging of the back 
and chest, while the child sits in a warm bath, is very helpfid. 

2. Spasmodic Croup is an affection of children from two to five 



DISEASES OF THE BRONCHI 



7 



years of age. Often it is part of an acute catarrhal laryngitis, in other 
cases it appears to be an independent disease. The presence of adenoids 
or enlarged tonsils predisposes a child to this disease. The child having 
been a little hoarse in the afternoon, or perhaps perfectly well, falls 
asleep as usual, to wake during the evening or late at night with a 
hoarse, croupy cough and some dyspnea. In the milder cases the dis- 
turbance is slight and the child quickly falls asleep again. In the 
severer cases the cough persists, the dyspnea increases, cyanosis develops, 
with retraction of the suprasternal and infracostal regions, in fact aU 
the symptoms of laryngeal stenosis. Sooner or later the attack subsides, 
the child falls asleep, and wakes in the morning perfectly well or with 
only a slight hoarseness. The attack may be repeated on several succeed- 
ing nights. Recovery always occurs. 

Diagnosis. — It is important to distinguish this affection from 
diphtheritic laryngitis. This is usually easy from the suddenness of 
the onset, the promptness of relief under appropriate treatment, 
and the absence of any diphtheritic lesion of the tonsils or pharynx, yet 
mistakes are made from time to time with very serious results. A culture 
should always be made from the throat, as the safest means of 
differentiation. 

Treatment. — For the attack the syrup of ipecac, one-half to one 
teaspoonful, repeated till vomiting is produced, is usually sufficient. 
Inhalations of chloroform are also effective. Steam inhalations or a 
hot mustard foot-bath may serve in mild cases. Enlarged tonsils and 
adenoids should be removed. 

DISEASES OF THE BRONCHI 

ACUTE BRONCHITIS 

Definition. — An acute catarrhal inflammation of the mucous mem- 
brane of the bronchi. It is frequently associated on the one hand with 
tracheitis, on the other with an inflammation of the finer bronchi, the 
so-called capillary bronchitis. 

Etiology. — Bacteria are the active agents. Many are normally pres- 
ent in the bronchi, such as strepto-, staphylo- and pneumo-cocci. Fried- 
lander's bacillus. Certain conditions favor the action of bacteria: (1) 
The invasion of acute infectious diseases, especially measles, influenza, 
whooping-cough, typhoid fever, and tuberculosis. Possibly the specific 
agents of these diseases are the direct excitants of the bronchitis. (2) 
Influences lowering the vitality or resistance of the patient: (a) Old 
age and childhood, (b) Exposure to cold and wet. The winter months 
are, therefore, the favorite season for bronchitis. (c) Sedentary or 
indoor life, (d) Various diseases, such as Bright 's disease or gout. (3) 
Influences directly influencing the bronchial mucous membrane: (a) 
Extension of a eoryza or laryngitis. Bronchitis is frequently the sequel 
of an inflammation beginning in the nose or throat, (b) Inhalation of 
dust, or irritant vapors, such as bromine or formalin, (c) Adenoids and 



8 DISEASES OF THE RESPIRATORY TRACT 



enlarged tonsils by causing month-breathing lead to freqnent attacks 
of bronchitis. 

Pathology. — The affected portions of the mucons membrane are con- 
gested, swollen, and covered by an abundant mucons or mucopurulent 
secretion. Microscopically desquamation of epithelium, edema of the 
mucosa and submucosa, possibly infiltration with leucocytes may be 
demonstrated. 

Symptoms. — The onset of acute bronchitis may be either gradual or 
sudden. The characteristic symptoms are cough and expectoration. The 
cough is usually frequent, harsh and paroxysmal. The expectoration is 
mucous or mucopurulent, scanty at first, becoming more abundant and 
more purulent as the bronchitis subsides. Infants and young children 
do not expectorate, but raise the mucus into the throat and then swallow 
it. Severe bronchitis may give rise to pain under the sternum, especially 
after coughing, or in either hypochonclrium from straining of the dia- 
phragm and abdominal muscles. In vigorous adults constitutional symp- 
toms are lacking or limited to slight fever and malaise. In children and 
the aged acute bronchitis may be severe, with fever of 102^ to 103°, 
rapid pulse, some dyspnea, possibly cyanosis, loss of appetite, and marked 
prostration. The physical signs consist of rales, which may be crepitant, 
subcrepitant, coarse, or piping, either localized or heard diffusely over 
both lungs. 

Course. — The fever and constitutional sj^mptoms should subside 
within a week or ten days ; the cough and expectoration may then disap- 
pear or they may continue for several weeks. The severer cases, 
especially in children and the aged, may readily develop into broncho- 
pneumonia. 

Diagnosis. — The symptoms and physical signs combined make the 
diagnosis easy. We must remember that an acute bronchitis often ushers 
in measles, whooping-cough, or typhoid fever. In every protracted case 
tuberculosis must be excluded by careful observation, examination of 
the sputum, and, if necessary, tuberculin tests. Infiuenza may be dis- 
tinguished only by the severer constitutional s^^mptoms or by the demon- 
stration of Pfeiffer's bacillus in the sputum, although, as stated under 
infiuenza, the latter is often lacking in cases classed as influenza. 
Examination of the sputum in acute bronchitis shows it to be composed 
of mucus, desquamated epithelium, leucocytes or pus cells, and bacteria. 
The organisms commonly found are the streptococci, staphylococci, pneu- 
mococci, and Friedlander 's bacillus. 

Treatment. — ]\Iild cases often go untreated or require only a sedative 
cough mixture to relieve the cough at night. Severer cases may be treated 
at the onset by a hot bath, hot drinks and Dover's powder, as described 
under coryza. Rest in bed for several days should then be required. 
The diet should be light and the bowels kept open by laxatives. Counter- 
irritation by camphorated oil for children or by mustard pastes, one 
part mustard to three or four parts flour, for adults helps to relieve con- 
gestion and al]ay coni^h. For scanty expectoration and freqnent cough. 



DISEASES OF THE BRONCHI 



9 



inhalations of steam with, compound tincture of benzoin are useful. The 
use of the many cough mixtures is steadily diminishing, because they so 
frequently nauseate the patient and interfere with feeding, which is of 
the utmost importance. In the early stages small doses of codein (gr. 14) 
or heroin (gr. K2-K6) may be given to adults when necessary to allay 
the cough and permit sleep. Sedatives of this kind possibly increase 
the danger of bronchopneumonia and should be given with caution to 
children or the aged. In the late stages stimulating expectorants such as 
ammonia, senega or squills may be employed. Change of air to a milder 
climate will often hasten the cure. Cod liver oil and other tonics are of 
value in convalescence. 

CHRONIC BRONCHITIS 

Definition. — A chronic inflammation of the bronchi, usually the 
larger and medium-sized tubes. 

Etiology. — (1) Repeated attacks of acute bronchitis. (2) Chronic 
congestion due to heart disease, or diseases of the lungs, such as emphy- 
sema and tuberculosis. (3) Constitutional diseases, such as gout and 
chronic nephritis. (4) Mouth-breathing from adenoids or other causes. 

Morbid Anatomy. — The walls of the bronchi are thickened by 
chronic inflammation or thinned by dilatation. The mucous membrane of 
the bronchi shows desquamation or ulceration. The lesions of the asso- 
ciated diseases are found. Emphysema and bronchiectasis regularly ac- 
company the condition. 

Symptoms. — Chronic cough and expectoration are the chief symp- 
toms. (1) The cough is usually worse in the morning, owing to the 
accumulation of secretions during the night. Once the bronchi have been 
emptied, relief is had for some time, possibly for the day. During the 
summer the cough improves, or disappears, only to return with cold 
weather and renewed attacks of acute bronchitis. During the exacerba- 
tions the patient may have fever. (2) The expectoration may be vers^ 
slight, the so-called dry catarrh, or so abundant as to merit the designation 
of bronchorrhea. In some cases it becomes putrid. It is regularly most 
abundant in the morning. (3) Dyspnea develops sooner or later from 
the accompanying bronchiectasis and emphysema. In the later stages 
the right heart fails with increasing dyspnea, cyanosis and anasarca. 

Course. — The disease is protracted through many years, possibly for 
the lifetime, with improvement in summer, relapses or exacerbations in 
wdnter. Recovery in the early stages is not difficult. 

Physical Signs. — In the milder cases there may be no abnormal 
signs on examination. Usually there are subcrepitant, sibilant or 
sonorous rales to be heard, especially over the lower and posterior parts 
of the chest. In advanced cases there may be the signs of bronchiectasis, 
emphysema and dilatation of the right heart. 

Diagnosis. — Tuberculosis must be excluded by repeated examinations 
of the sputum, possibly by tuberculin tests. Asthma can be recognized 
by the history of the patient and the paroxysmal dyspnea. Emphysema 



10 



DISEASES OF THE RESPIRATORY TRACT 



gives characteristic physical signs. The possibilit}' of the presence of 
an aneurism or tumor pressing on the bronchi must be remembered. 

Treatment. — A mild and equable climate is ad\dsable. The colder 
months of the year should be spent in Florida, Southern California, 
Arizona, or the South of France. Warm clothing and avoidance of 
exposure are important. Careful attention must be given to the digestion 
and general health of the patient. For the cough itself many remedies 
are used. Full warm baths are recommended. A combination of sodium 
bicarbonate 15 grains, sodium chloride 5 grains, spirit of chloroform 5 
minims, in anise water may be given in warm milk or water for the morn- 
ing cough. Terebene in ten minim doses, creosote in 2 or 3 minims, or 
terpene hydrate 2 to 5 grains, may be given three or four times a day. 

FIBRINOUS BRONCHITIS 

Definition. — A rare disease, of either acute or chronic course, char- 
acterized by paroxysms of dyspnea and cough in which casts of some of 
the bronchi are expelled. 

Etiology. — The disease may be idiopathic or occur as a complication 
of various infectious diseases, such as diphtheria, pneumonia, measles, 
scarlet fever, erysipelas, typhoid, variola, rheumatic fever, or influenza. 
The diphtheria bacillus, the pneumococcus and various other organisms 
have been found in the casts. 

Morbid Anatomy. — The casts represent moulds of small parts of the 
bronchial system as a rule ; in rare cases the whole bronchial system may 
be reproduced. They are composed of mucin or fibrin. 

Symptoms. — The clinical picture is that of a bronchitis, either acute 
or chronic, in which from time to time occur paroxysms of dyspnea and 
cough during which the casts are coughed up. Fever occurs intermit- 
tently during the course of the disease. The expulsion of the casts may 
be followed by free hemorrhage. 

Diagnosis. — The casts alone identify the disease. The presence of 
diphtheria or pneumonia must be excluded. 

Prognosis. — In the idiopathic form death is rare, in the secondary 
type it is not infrequent. There is a marked tendency to recurrence. 

Treatment. — The treatment is that of bronchitis, acute or chronic. 
Inhalations of steam or the volatile oils are reconunended. 

BRONCHIECTASIS 

Definition. — A local or general dilatation of the bronchi. 

Etiology. — This condition is never primary, but results from two 
factors: (1) inflammation of the walls of the bronchi, as in broncliitis 
or bronchopneumonia, weakening all the tissues of the wall; (2) increased 
intrapulmonary pressure, such as is caused by cough. The condition, 
therefore, follows (1) bronchopneumonia, especially in influenza or 
whooping-cough, or tuberculosis; (2) chronic bronchitis and emphysema: 
(3) compression of the bronchi by tumors or aneurism; (4) impaction of 



DISEASES OF THE BRONCHI 



11 



a foreign body in a bronchus; (5) interstitial pneumonia and chronic 
pleurisy. The disease is met with at all periods of life. 

Morbid Anatomy. — The dilatation is found localized or distributed 
generally through one or both lungs. The dilatations are fusiform or 
saccular. In some cases cavities of large size are produced, the cavities 
full of mucopurulent, possibly fetid, secretion. Emphysema, some 
sclerosis of the lung, and possibly chronic pleurisy are frequent 
accompaniments. 

Symptoms. — As a sequel or accompaniment of the conditions named 
above the patient develops a chronic cough with abundant, foul, or fetid 
expectoration. The cough is paroxysmal, occurring in the morning or 
at other times when the dilated bronchi become full. Once they are 




Fig. 1. — "Clubbed fingers" in a patient having bronchiectasis. From the collection of 
Dr. Vv^ alter B. James. 



emptied the cough ceases for some hours, possibly for the day. 
Paroxysms of cough and offensive secretion may make the patients 
wretched both in body and mind. The sputum is thin, mucopurulent in 
character, often foul in odor, and may amount to a pint or two a day. 
It contains great numbers of bacteria, degenerated leucocytes and epi- 
thelium, crystals of fatty acids, and possibly leucin and ty rosin. The 
disease lasts indefinitely. Mild cases may recover, the severer go on for 
years till the patient dies of exhaustion, from bronchopneumonia, or other 
complication. 

The physical signs are those of a localized bronchitis with subcrepi- 
tant or large mucous rales, or those of small cavities, at one time full of 
secretion, giving rise to dulness and diminution or absence of voice and 
breath sounds, and again empty and giving the usual signs of cavity. 

As in many other chronic pulmonary diseases, the terminal phalanges 



12 . DISEASES OF THE RESPIRATOEY TRACT 



of the fingers may show enlargement, which by the X-ray can be shown to 
affect only the soft tissues. (See Fig. 1.) 

Diagnosis. — The character of the cough and expectoration usually 
marks the condition. The physical signs other than the rales are often 
difficult to obtain. Tuberculosis must be excluded by the absence of 
constitutional symptoms, failure to find the bacilli in the sputum, and 
possibly by tuberculin tests. 

Treatment. — The milder cases are treated as cases of chronic bron- 
chitis. Residence in a mild, dry climate is of most value. Intratracheal 
injections of menthol 10 parts, guaiacol 2 parts, and olive oil 88 parts, 
are recommended. Single bronchiectatic cavities in accessible positions 
may be opened and drained surgically. 

BRONCHIAL ASTHMA 
(Spasmodic Asthma ) 

Definition. — No satisfactory definition of the affection can be given. 
The term astlnna is often applied to dyspnea of renal or cardiac origin, 
but should be applied only to the affection here described. 

Etiology. — The affection occurs at all ages, most often in males, and 
especially in persons of neurotic ancestrj^ Liability to the disease is 
hereditary in some families. Certain nasal conditions, such as nasal 
polypi, hypertrophic rhinitis, or adenoids, predispose to it. Hay fever 
and asthma are closely allied and often associated. In persons subject to 
astlnna the attacks are precipitated by a great variety of causes; the 
exciting cause is often peculiar to the individual. To one, residence in 
the city is harmful, to another the country. The odor of certain flowers, 
or animals, or the pollen of certain plants will cause attacks in some 
cases and not in others, and so on. Fright or excitement of any kind, 
exposure to cold or wet, disturbances of digestion and the like, are all 
given as possible causes of attacks. 

TpiEORiES.'i— There are several theories of the causation of the dyspnea : 
(1) Spasm of the muscular coats of the smaller bronchi. (2) A special 
form of inflammation or swelling of the bronchial mucous membrane, 
with a peculiar exudation, the bronchiolitis exudativa of Curschmann. 

(3) Spasm of the diaphragm and possibly of other muscles of respiration. 

(4) The phenomena excited by injections of foreign serum in animals 
already sensitized by previous injections sometimes closely resemble 
asthma. In man paroxj^sms of severe or even fatal asthma have been 
precipitated by injections of diphtheria antitoxin (horse serum). This 
accident has occurred especially in those who have previously suffered 
from astlnna. Meltzer has suggested that asthma is therefore an anaphy- 
lactic reaction excited in sensitized persons by inoculation with foreign 
albumins (pollen, etc.). 

Symptoms. — The attacks of dyspnea, Avhich constitute the essential 
featiii-c in asthma, come suddenly without Avarning, or may be pi'eceded 
by disturbances of digestion, nervousness, or depression which enable the 



DISEASES OF THE BRONCHI 



13 



patient to foretell an attack. Nocturnal attacks are frequent. In the 
milder attacks the patient suffers only slight dyspnea and an annoying 
cough with tenacious expectoration. In the typical form the dyspnea 
is extreme, the patient sits up, supporting the shoulders by clasping the 
arms of a chair or resting the elbows on a table, in order to give more 
effective play to the accessory muscles of respiration. Inspiration is 
quick and jerky, all the muscles of respiration, excepting the diaphragm, 
which is rigid, being throAvn into violent action. The muscles of the 
neck especially stand out. Despite the effort, but little air enters the 
chest. Expiration is prolonged to several times the normal time. Both 
inspiration and expiration are accompanied by loud wheezing and piping 
sounds which may be audible at some distance from the chest. The total 
number of respirations per minute is little, if at all, increased, and the 
pulse is but little disturbed. The face is pale, or livid, frequently 
bathed in cold sweat, the expression anxious, speech difficult or impos- 
sible, and in severe cases death seems inevitable. Sooner or later, 
however, the spasm relaxes, air enters the chest more easily and the attack 
after lasting tw^o or tlrree hours subsides. Usually some dyspnea remains 
for several days and the severe symptoms recur at any time. During 
the critical period there is little or no expectoration. With relaxation 
the patient coughs and expectorates freely. The sputum is thick, tena- 
cious, consisting chiefly of mucous plugs or masses. Floated in water, 
these masses may show the form of Curschmann's spirals. Micro- 
scopically the sputum shows numerous eosinophile cells and possibly the 
Charcot-Leyden crystals. The spirals consist of mucin ; the composition 
of the crystals is unknown. The blood shows a leukocytosis and an eosino- 
philia. The paroxysms of asthma may be repeated for days or weeks. 
Usually after a paroxysm the patient is free for weeks or months, till an 
attack is brought on again by some of the exciting influences. In chronic 
cases the patients regularly develop emphysema and chronic bronchitis. 

Prognosis. — The asthmatic attack is practically never fatal and yet 
the disease recurs through life. In some the attacks tend to increase in 
frequency, in others with care they can be made less frequent. 

Treatment. — For the paroxysm a hypodermic injection of morphine, 
Ve to 14 grain, usually gives relief. Atropine may be given with it. 
Of recent years remarkable success has been obtained from the hypo- 
'dermic use of adrenalin chloride, 10 minims of the 1/1000 solution being 
given. The fumes of stramonium leaves, in powder or cigarettes, may 
give relief. Nitre paper is similarly used. In the intervals careful ex- 
amination of the nose and throat must be made and adenoids or enlarged 
tonsils, nasal polypi or hypertrophied turbinates removed. The general 
health must be improved by attention to diet and manner of life. Change 
of climate may relieve when other means fail. Each individual must 
select a place for himself, where he is free from attacks. The adminis- 
tration of iodide of potassium or arsenic may be tried. In some persons 
aspirin in doses of 10 grains two or three times a day will prevent at- 
tacks or afford relief during them. 



14 



DISEASES OF THE RESPIRATORY TRACT 



BRONCHOPULMONARY HEMORRHAGE 

Hemorrhage from the lungs, or hemoptysis, occurs from a great 
variety of causes. 

(1) Tuberculosis of the lungs, from the rupture of large or small 
vessels. Hemorrhage may be the initial symptom, or may occur at any 
time during the disease, and in chronic tuberculosis is not rarely the final 
event. (2) Other inflammatory lesions of the lungs, such as pneumonia, 
abscess, or gangrene, or even bronchiectasis or emphysema. (3) Con- 
gestion of the lungs from heart disease, especially lesions of the mitral 
valve, or from infarctions resulting from endocarditis. (4) Arterio- 
sclerosis affecting the pulmonary vessels, especially in the gouty. (5) 
New growths of the lung. (6) Trauma from blows upon the chest or 
falls, especially from puncture by broken ribs. (7) The strain of heavy 
lifting. (8) Aneurisms of the aorta or pulmonary vessels rupturing into 
the lung. Erosions in the bronchi may be caused by pressure of 
aneurisms and bleeding follow without actual rupture. (9) Pulmonary 
diastomatosis, invasion of the lung by parasitic flukes in Japan and 
China sometimes gives rise to hemorrhage from the lungs. (10) Ul- 
cerative lesions of the larynx, trachea, or bronchi. (11) Hemoptysis may 
occur in the hysterical and neurotic without discoverable cause. (12) 
Scurvy, leukemia, purpura, and the malignant types of acute infectious 
diseases, are sometimes complicated by hemoptysis. (13) Vicarious men- 
struation is a rare cause. (14) Finally pulmonary hemorrhage not 
infrequently occurs in young persons without discoverable cause and 
these individuals may never develop tuberculosis or any other disease to 
explain the occurrence. 

Symptoms. — The blood usually appears suddenly and unexpectedly. 
The patient feels a tickling in the throat, coughs, and expectorates blood. 
The amount brought up varies from a trace to a pint or more. Usually 
the actual amount of blood lost is small, possibly an ounce or two. The 
associated symptoms vary greatly. The patient may not be disturbed at 
all. Frequently they are greatly excited and anxious, the face flushed, 
the pulse rapid and bounding. Only in rare cases do they lose sufficient 
blood to give the constitutional symptoms of hemorrhage, pallor, breath- 
lessness, sweating, rapid, small and weak pulse, and corresponding 
depression. 

The physical signs vary with the cause. During the attack of hemor- 
rhage the usual examination of the chest should be omitted altogether, 
or limited to auscultation of the natural breathing. 

Diagnosis. — The chief point is to make sure that the blood comes 
from the lungs. Blood flowing from the nose may run into the throat 
and then be coughed up. The nose, throat, and larjrax should be care- 
fully examined. The stomach is the only other probable source. Blood 
from the lungs is bright red, frothy, alkaline. That from the stomach 
is regularly altered in some degree, mixed with food or mucus, probably 



DISEASES OF THE LUNGS 



15 



acid from such admixture, and often "coffee-grounds" in appearance. 
Search for the cause of the hemorrhage must often be postponed till all 
bleeding has ceased. The history of the patient, the conditions under 
which the hemorrhage occurred, and the results of physical examination 
will usually lead one to a correct conclusion. 

Prognosis. — Only in aneurism or in advanced tuberculosis is pul- 
monary hemorrhage likely to be fatal. The ultimate outcome depends 
upon the cause of the bleeding. In certain eases of pulmonary congestion 
due to heart disease hemorrhage from the lungs may give relief. 

Treatment. — Quiet of body and mind is essential. The patient should 
be put to bed and a hypodermic injection of morphine sulphate, 14 grain, 
given. Assurance as to the outcome of the hemorrhage is most valuable. 
If blood pressure be high, nitroglycerine may be given hypodermatically, 
or amyl nitrite inhaled. No other treatment is ordinarily called for. 
Eest should be continued till the bleeding has entirely ceased. 

DISEASES OF THE LUNGS 

DISTURBANCES OF CIRCULATION OF THE LUNGS 

Congestion of the lungs may be either active or passive. 

1. Active Congestion occurs (1) in the initial stage of pneumonia, 
bronchitis, pleurisy, or tuberculosis; (2) from the inhalation of ex- 
cessively hot or cold air or irritating gases; (3) from violent exertion. 
The symptoms and physical signs are those of the initial stage of pneu- 
monia, and the treatment the same. 

2. Passive Congestion. — Two forms are recognized: (a) Brown in- 
duration, the congestion of the lung brought about by disease of the 
heart, chronic endocarditis, myocarditis, or dilatation, which prevents the 
normal flow of blood from the lungs, or by pressure of aneurisms or 
tumors upon the pulmonary veins. The capillaries of the lung become 
distended, some diapedesis and hemolysis take place and chronic bron- 
chitis ensues. Cough and expectoration result and in the sputum leuco- 
cytes and epithelial cells containing blood pigment can be found. 

(b) Hypostatic Congestion is brought about partly by weakness of 
the heart action, partly by gravity, and is met with in all enfeebled states 
of the body and especially in the acute fevers, such as typhoid. It is 
marked in conditions associated with stupor or coma, such as brain 
lesions, or morphine poisoning. The posterior portions of the lungs are 
deep, bluish-brown in color, heavy, and dark blood flows freely on incision. 
Microscopically the veins and capillaries are engorged with blood, and 
blood is often found in many of the air-vesicles. Physical examination 
shows deficient pulmonary resonance over the bases of both lungs, with 
diminished voice and breathing sounds and many coarse, sometimes 
bubbling, rales. 

Treatment. — The condition should be prevented, if possible, by fre- 
quently turning any recumbent patient from one side to the other or 
upon the face, to prevent the settling of the blood in the posterior and 



16 



DISEASES OF THE RESPIRATORY TRACT 



lower parts. The heart action must be maintained by appropriate treat- 
ment. Cupping of the chest may be resorted to in extreme cases. 

Edema of the Lungs. — Exudation of serum into the lungs is rarely 
primary, but is a feature of the terminal stages of many diseases, espe- 
cially those of the lungs, the heart, arteries, and kidneys. It occurs espe- 
cially in patients who already have marked pulmonarj^ congestion with 
edema in other parts of the body. Not infrequently it follows too rapid 
removal of pleural effusions. One in every four or five deaths in cases 
of protracted illness is ushered in by pulmonar}^ edema. The lungs post- 
mortem are very heavy, sodden, and usually congested posteriorly. On 
section a watery serum exudes freeh^ from the cut surface, either clear 
or blood-tinged. The cause of pulmonary edema is found in increased 
blood pressure in the capillaries of the lungs, aided by degenerative 
changes in the capillary epithelium, possibly bacterial in origin. 

Symptoms. — Pulmonary edema usually comes on suddenh^ with 
urgent dyspnea, cough and expectoration of frothy watery fluid, if the 
patient is strong enough to cough and expectorate, cyanosis, rapid, irregu- 
lar and feeble heart action. Unless promptly relieved death is imminent. 

Phy^xCAl Signs. — The condition is regularly associated with hypo- 
static congestion, the signs of which are present, and in addition abundant 
loud, bubbling, liquid rales, which can be readily felt by the hand on 
the chest wall, as well as heard. These rales may be heard only at the 
bases or may be present over all parts of the lungs. The mouth and 
throat may be ^lled with bubbling watery mucus, and every respiration 
accompanied by bubbling, the traditional ''death rattle" of the novelist. 

Treatment. — Dry cupping of the chest, counter-irritation by mustard 
paste applied to the chest, and rapid cardiac stimulants, such as camphor, 
strj'chnine, caffeine, and alcohol, are indicated. Adrenalin cliloride, ten 
minims of the 1/1000 solution, has also been found effective. Artificial 
respiration may aid. Venesection may be employed if cyanosis and en- 
largement of the right heart are present. 

Embolism, Thrombosis, and Inf.vrction of the Lung. — Emboli from 
various parts of the body may lodge in the lung. The right heart, espe- 
cially the auricular appendix, is the most frequent source, but they may 
come from injury or disease of the bones (fat embolism), or from 
phlebitis such as occurs in the uterine or femoral veins. 

Morbid Anatomy. — A branch of the pulmonary artery having been 
plugged, if the patient lives, the territory supplied by the artery becomes 
an area of lowered blood pressure and blood from all the adjacent areas 
settles in it till it becomes intensely engorged and even infiltrated with 
blood, producing the infarction. Later the blood is absorbed and the 
infarction becomes an area of fibrosis or scar tissue. If large branches 
of the pulmonary artery are plugged, the patient dies so promptly that 
nothing more than the thrombus or embolus is to be found. 

Infarcts appear as wedge-shaped or globular areas, firm, deep-red or 
blackish-red in color, oozing blood on section. Microscopically blood is 
found ill the air- vesicles and infiltrating the interstitial tissue. Finally 



DISEASES OF THE LUNGS 



17 



only the areas of scar tissue are left. In cases of fat embolism there may 
be great numbers of plugs of fat found in the finer branches of the pul- 
monary artery. 

Etiology. — Pulmonary embolism is a frequent complication of eudo- 
carditis, especially the malignant type. It may follow metritis, or typhoid 
fever, or injury (fracture) or disease involving the medulla of bones. 
It is one of the causes of sudden death following operations upon the 
appendix, uterus, or other abdominal organs. 

Symptoms. — With embolism of a large vessel, death follows almost 
at once with symptoms of sudden dyspnea, cyanosis, and great anxiety. 
Smaller emboli give rise to some pain in the side, dyspnea, cough, and 
expectoration of blood. The symptoms may be of brief duration or con- 
tinue for several days, depending on the size of the obstructed vessel. 

Physical Signs. — In the quickly fatal cases no local signs are ob- 
tainable. In other cases the infarction may be represented by an area 
of dulness, at the base of a lung or in the axilla, with diminished voice 
and breathing ; or, if the area be large, bronchial voice and breathing, and 
fine, subcrepitant or coarse rales. 

Diagnosis. — Pneumonia gives similar signs, but the absence of the 
constitutional symptoms usually renders the diagnosis easy. The seqiT^nce 
of events also usually points directly to embolism. 

Treatment is purely symptomatic, for relief of pain and distress. 

ATELECTASIS 
(Pulmonary Collapse and Compression) 

Atelectasis, or failure of expansion in the lungs of the ne born, is 
frequently seen in infants who have been asphyxiated during birth or 
are enfeebled by prematurity or other cause. If the atelectasis is ex- 
tensive, the infants are cyanotic and breathe feebly, the cry is weak, the 
pulse is rapid, and they are liable to attacks in which the cyanosis becomes 
extreme, and death may ensue. 

Collapse of the lungs is a similar condition, occurring in children or 
adults, as the result of obstruction of the finer bronchi by secretions 
accumulating in them from bronchitis or bronchopneumonia or by 
pressure upon them caused by tumors or pleural effusions. The extreme 
grades of the condition , such as are seen when an entire lobe or lung is 
compressed by a pleural effusion have been spoken of as carnification. 

In atelectasis and collapse the non-aerated portions of the lungs 
appear as depressed areas on the pleural surface, deep red or bluish in 
color from congestion, extending a varying distance into the substance 
of the lung. With a blow-pipe such areas can l)e readily inflated and 
made to appear normal. 

Physical Signs. — In infants atelectasis rarely gives appreciable pul- 
monary signs. Theoretically there should be sliglil dulness over the lungs 
posteriorly, but the change is too slight to be of imi^oiiance. Colla])se of 
the lung in older children is usuall\' obscured by llu^ signs of bi'onchitis or 
bronchopneumonia. It may serve to lessen pulmonary resonance and make 
2 



18 



DISEASES OF THE RESPIRATORY TRACT 



the breathing and voice signs faint. The compressed lung, if the area is 
large, gives dulness and diminished or absent voice and breath sounds. 
It is usually the chief factor in the continuance of the signs after re- 
moval of fluid. 

Treatment. — Atelectasis in new-born infants must be treated by main- 
taining the body heat, and from time to time stimulating respiration by 
sprinkling alternately hot and cold water upon the chest, or by spanking. 
Direct inflation of the lungs has not been successful, and medication is 
of little value. 

In children and adults collapse of the lung is to be prevented, if pos- 
sible, by the adequate treatment of bronchitis or bronchopneumonia, or 
the removal of effusions. In bronchitis or bronchopneumonia measures 
directed to the removal of secretions from the bronchi are of value. 
Frequent changes of position, especially turning on the face, or lifting 
the foot of the bed, help drainage. Stimulating expectorants, such as 
ammonium carbonate or chloride, may be of value. Vomiting may be 
produced in patients not too debilitated. 

In cases where the lung has been compressed by effusions, after the 
removal of the fluid or drainage of the chest, expansion of the lung may 
be favored by respiratory exercises. Forced inspiration may be prac- 
ticed at intervals during the day, either normally or with compression of 
the sound side. Wolff's bottles, in which water is blown from one to 
the other, may be used. 

LOBAR PNEUMONIA 
(Croupous or Fibrinous Pneumonia. Lung Fever ) 

Definition. — Primary lobar pneumonia is a specific infectious disease 
marked by a local inflammatory lesion in the lung, a general toxaemia 
and a sharply self -limited febrile course. 

Etiology. — Predisposing Causes. — Pneumonia is among the com- 
monest of acute diseases and is widely spread throughout the world, 
although most frequently encountered in temperate climates. It occurs 
chiefly during the cold, wet months of the year and is most prevalent 
in the late winter and spring. No age is exempt, but the disease is com- 
monest in children of between two and six years, in adults of between 
twenty and forty years, and in the aged. ]\Iales are more frequently at- 
tacked than females. The sudden lowering of vitality by exposure to cold 
is an important predisposing cause. IMalnutrition, alcoholism, overcrowd- 
ing and chronic diseases also increase the liability to pneumonia. The 
disease sometimes follows directly upon contusions and other injuries of 
the chest wall. One attack so far from conferring immunity seems dis- 
tinctly to predispose to further attacks and tAVO or more repetitions of 
the disease are by no means rare. 

The Exciting Cause. — Lobar pneumonia, in the vast majority of 
cases at least, is caused by a specific germ known variously as the diplo- 
coccns pneumonier, micrococcus la}iceolotus and pneumococcus. Its rela- 



DISEASES OF THE LUNGS 



19 



tion to the disease was made clear by the work of Fraenkel in 1884 and 
later by Weichselbaum. 

The DiPLOCOCCUS pneumonia is an oval or lance-shaped coccus occur- 
ring in pairs, with each pair usually surrounded by a faint capsule. The 
organism is found abundantly in the sputum of pneumonia patients, in 
the bronchi, in the inflamed areas of the lungs, in the complicating lesions 
of pleura, endocardium, pericardium, joints, etc. Moreover, it has been 
demonstrated recently that the germ is present in the circulating blood in 
most if not all cases during the active stage of the disease. The pneu- 
mococcus is also found not infrequently in the mouths of healthy indi- 
viduals, is capable of producing many other inflammations than those 
of the lungs and may even cause a general septicaemia without evident 
local lesion. The harmful effects of the organism seem to be due chiefly 
to the production of an active toxin — the so-called pneumotoxin — which 
is present in the blood during the active stage of pneumonia. The germ 
probably reaches the lung through the respiratory passages, but some- 
thing more than its mere presence there {e.g., lower resistance of the 
tissues or increased virulence of the germ) is needed to produce the 
disease. 

It is true that other micro-organisms than the pneumococcus {e.g., 
Friedlander 's bacillus, B. influenz£e, B. typhosus, etc.) seem capable of 
exciting similar inflammations of the lungs, but there can be no doubt 
that most, if not all cases, of primary lobar pneumonia are due to infec- 
tion by the diplococcus pneumonia?. 

Although usually the disease seems but slightly transmissible, its con- 
tagious nature is sometimes clearly evident and many small, and a few 
large, epidemics have been recorded. 

Morbid Anatomy. — Usually the greater part, or the whole, of one 
lobe is involved in the inflammatory process. Not infrequently, however, 
two lobes of the same lung are affected, and occasionally one or more 
lobes of both lungs. The lower lobes are much more commonly attacked 
than the upper, and the right lung rather more frequently than the left. 
The inflammation is characterized especially by the preponderance of 
fibrin in the exudate. The process is divided into four stages. 

1. Stage of Engorgement. — The affected part of the lung is dark red, 
congested and somewhat firmer and heavier than normal, but still con- 
tains some air and floats in water. Its cut surface exudes blood. Micro- 
scopically the capillaries are seen to be greatly distended with blood. The 
air vesicles are small and contain only swollen alveolar cells and a few 
red cells. 

2. Stage of Red Hepatization. — The lung is now solid, very heavy and 
of a dull red color. It contains no air ;ind sinks in water. The pleural 
surface is covered with fibrinous exudate ; the cut surface is dry, gran- 
ular, of brick red color. Microscopically the alveoli are seen to be dis- 
tended with a thick mesh-work of fibrin cTiclosing red cells, desquamated 
epithelial cells, leukocytes ])n(Miiii()('()('(M. 'I'Ik^ infundibula and many 
of the finer bronchioles also are filled with exudate. 



20 



DISEASES OF THE RESPIRATORY TRACT 



3. Stage of Gray Hepatization. — The inflamed area is still solid and 
unaerated but has now a grayish or yellowish gray color and is extremely 
friable. The cut surface is no longer dry and gTanular. but exudes a 
thick, turbid fluid. The microscope shows the alveoli still distended and 
the capillaries collapsed, but the exudate is no longer chiefly made up of 
fibrin net- work and red cells. These have, for the most part, disappeared 
and the exudate consists chiefly of polymorphonuclear leukoc}i:es, gran- 
ular detritus and serum. 

4. Stage of Besolution. — The lung becomes less and less solid, the 
alveoli again contain air, the disintegration, liquefaction and absorption 
of the exudate continue until the lung tissue is completely restored to 
integrity. In the disappearance of the exudate expectoration plays no 
appreciable part. The removal is brought about by absorption and by 
the action of the phagocytic leukocytes. 

The different stages described are by no means always sharply defined, 
and it is not uncommon to have red and gray hepatization at the same 
time in different parts of the same lobe. 

Symptoms. — The ixcubatiox period is net known, but is usually not 
longer than a day or two. 

The ONSET is regularly abrupt, a severe cliill being usually the first 
symptom. Occasionally cough, fever or pain in the chest may precede 
the chill by a few hours. Occasionally, too, a distinct rigor may be lacking. 
The temperature rises within a few hours to 103^ or 104° F. and remains 
continuously high. There are the usual headache, prostration and gen- 
eral pains of a severe acute infection. Pain in the chest and a short, 
dry cough are early and, usually, distressing symptoms. The patient 
is apt to lie on the affected side, and with his flushed cheeks, bright eyes, 
anxious expression and rapid breathing presents a very characteristic 
and distinct picture. The fever rises abruptly with the chill and within 
12 hours usually reaches 103°-105° F. This height is thereafter main- 
tained throughout the disease with little variation ; the fever chart show- 
ing a striking contrast to the regular daily fluctuations seen in typhoid. 
Some time between the fifth and the ninth day of the disease, most com- 
monly on the seventh day, the temperature suddenly drops within a 
few hours to normal or thereabouts. This crisis is one of the striking 
features of pneumonia and is usually accompanied by a profuse sweat 
and by great amelioration of all the symptoms. Not all cases show this 
sudden and violent drop. Often the critical fall occupies 24 or 36 hours 
and sometimes, especially in children, the descent is more gradual still — 
by lysis. Rarely the crisis is seen as early as the third day or is delayed 
until the eleventh or twelfth day. Occasionally a sharp but temporary 
drop in temperature (pseudo-crisis) occui^ a day or two before the true 
crisis. Among the aged the fever is apt to be low. (See Figs. 2 and 3.) 

The coi^GH is a prominent and often a distressing symptom. It is at 
first short, hard, painful and unproductive. Soon, however, it is accom- 
panied hy scanty, tenacious, blood-stained sputum. The blood may at 
first ap])('Mi' in 1)riuht streaks. ])ut it usually shows as a brick red or 



DISEASES OP THE LUNGS 



21 



orange tinge, and these small, tough, rust-colored sputa are among the 
important diagnostic signs of the disease. In the later stages the ex- 
pectoration becomes more abundant, mucopurulent, and faintly yellow 
or green in color. 

Pain begins usually within a few hours of the onset, is referred as 
a rule to the axilla of the affected side, is sharp and stabbing in character 
and is made much worse by a deep breath or by coughing. It is apt to 
subside in the latter part of the disease, but it may remain intense and 
distressing throughout. Occasionally it is lacking altogether. Rarely the 
pain may be referred chiefly to the abdomen. 

Dyspnea. — The breathing rate is increased from the beginning. At 
first the increase is only moderate (30-40 per minute) ; later on in the 
disease, however, especially if the case be doing badly, the rate may reach 




Fig. 2.— Fever of lobar pneumonia. The remissions of the fever are somewhat more marked than 

is usual. 

50 or 60 or even more. At such times the breathing is labored and is 
attended with cyanosis. In children and some adults expiration is com- 
monly accompanied by an audible grunt. 

The PULSE at first is full, bounding, of low tension and moderately 
increased in rate (100-110). As the disease progresses the rate some- 
what increases and the size and force of the pulse lessen. In grave cases 
the rate may reach 140 or 150. The heart action shows corresponding 
variations. The sounds at first are loud and clear, but grow progressively 
fainter as the heart weakens. The second pulmonic tone is usually ac- 
centuated and a progressive weakening of this sound is a warning of 
value as indicating failing strength in the right ventricle. In fatal cases 
the heart grows progressively weaker and more rapid; the lips, nails and 
skin generally take on a bluish tinge; pulmonary edema develops; the 
skin is bathed in cold sweat; cyanosis becomes more and more marked 
and the patient gradually sinks into stupoi- and dies. 

The BLOOD shows regularly a leukocytosis and an increase in the fibrin 
constituents. The leukocytes vai'V usually between 12,000 and 30,000 



22 DISEASES OF THE RESPIEATORY TEACT 



per c.mm., but may reach 60,000. The increase affects especially the 
polymorphonuclear cells, which may form 90-95 per cent, of the total. 
The absence of a leukocytosis is usually an unfavorable symptom. 

Nervous Symptoms. — In children a convulsion may replace the initial 
chill. Delirium occurs under several conditions. It is common in the 
pneumonias of children, in adults with very high fever, in cases compli- 
cated by meningitis and especially in alcoholic subjects. It is usually 
of the noisy, violent type. In debilitated subjects and in the aged, how- 
ever, the delirium is often quiet and muttering. 

Digestive symptoms are as a rule not prominent. The tongue is 
usually heavily coated and moist, but in many of the severe cases becomes 
.dry, brown and cracked. Vomiting is not uncommon at the onset and 
may persist. Constipation is the rule, but diarrhea is not very infre- 




FiG. 3. — Lobar pneumonia with a pseudo-crisis on the third day, a rise of fever again on the fifth 

day, with a final fall. 

quent. An occasional and very grave symptom is the appearance of 
marked tympanitic distention of the abdomen. Jaundice, usually of the 
non-obstructive type, is sometimes seen. 

The URINE during the active stage of the disease is concentrated, 
highly colored, usually contains a small quantity of albumin and is 
deficient or altogether lacking in chlorides. 

An eruption of herpes around the lips and nose occurs in about one- 
half of the cases. 

Physical Signs. — These differ so much at different periods of the 
disease that it is convenient to describe them separately in the stages of 
engorgement, hepatization and resolution. 

In the FIRST STAGE (engorgement) inspection shows the flushed 
anxious face, the rapid breathing, the movement of the ala? of the nose 
and, usually, slight restriction of movement of the affected side of the 
chest. By palpation this limitation of movement is even better appre- 
ciated. Vocal fremitus is usually not distinctly changed from the normal, 
])iit may be slightly increased. A pleural friction rub is sometimes felt. 



DISEASES OF THE LUNGS 



23 



Percussion reveals some impairment of normal resonance when compared 
with the other side. This slight dulness is often accompanied by a dis- 
tinctly tympanitic quality — the so-called Skodaic resonance. By auscul- 
tation one can detect over the affected area usually a distinct enfeeble- 
ment or actual suppression of the normal vesicular murmur. Sometimes, 
however, the breath sounds are harsh and approach the bronchial type 
(broncho-vesicular breathing). The transmitted voice is often louder 
and clearer than normal, but is not distinctly bronchial. A sign of much 
importance is the crepitant rale which is heard regularly during this first 
stage. It consists of a group of very fine, dry, crackling sounds at the 
end of inspiration. This stage usually lasts one or two days. 

Stage of Hepatization. — Inspection and palpation show much re- 
striction of movement over the affected portion and exaggerated move- 
ment of the other side. Vocal fremitus is distinctly increased. On per- 
cussion there are dulness, amounting often almost to flatness, and marked 
resistance to the examining finger. If the apex is involved the note has 
often a tympanitic quality as well. 

Auscultation reveals complete disappearance of the normal vesicular 
murmur and its replacement by a loud, high pitched bronchial sound both 
on inspiration and expiration. The voice is greatly intensified and clear 
(bronchophony), as is also the whisper. Hales are usually lacking in 
this stage. 

Stage of Hesolution. — With the beginning of resolution there is a 
gradual return of all the signs to normal. The chest moves more freely 
and the percussion note becomes less and less dull (although it may be 
some time before it is perfectly resonant) . The bronchial breathing grows 
softer and lower pitched, is audible only with expiration and finally is 
replaced by the vesicular murmur. The rales return in this stage and 
are usually very abundant. Some are of the crepitant type, but most of 
them are moist rales of different degrees of coarseness. They are heard 
chiefly with inspiration. 

Variations in Physical Signs. — The signs of the first stage may last 
but a few hours or may be protracted for several days. Indeed, dulness 
and bronchial breathing may be lacking altogether, if the consolidation 
is small and is deep in the lung. Bronchial breathing is absent also in 
cases where the bronchi are occluded by mucus or by fibrinous exudate 
(massive pneumonia). 

The signs of resolution usually appear about the time of the fall in 
temperature, but sometimes resolution is almost completed before the 
crisis occurs. On the other hand, resolution may be much delayed and 
dulness and bronchial breathing may persist for some days or even weeks 
after the temperature has fallen. A complicating pleural affection may 
greatly modify the physical signs and lead to much confusion. 

Special Forms. — The term double pneumonia is applied to cases 
in which both lungs are involved. If the consolidation is small and deep- 
seated (central pneumonia) the physical signs are apt to be slight and 
indistinct and very slow in developing. Instances of massive pneumonia 



24 



DISEASES OF THE RESPIRATORY TRACT 



are seen rarely in which not alone the lung parenchyma but the bronchi 
as well are filled Avith fibrinous exudate. The transmission of the bron- 
chial breath and voice sounds is thus prevented and these important signs 
may be altogether lacking. 

Creeping or migratory pneumonia is that form in which the inflam- 
matory process attacks various portions of the lung in succession. 

When, after the usual onset, the disease subsides in the course of two 
or three days without going on to its full development it is spoken of as 
LARVAL pneumonia. An important form is that known as asthenic or 
TOXIC pneumonia in which the symptoms of toxemia are marked and out 
of all proportion to the extent of the local process. This type is common 
in aged and debilitated subjects and in drunkards. 

The term cerebral pneumonia is sometimes applied to cases in which 
the nervous symptoms are conspicuous. Such cases may closely simulate 
meningitis. 

Secont)ary pneumonias occur as a complication of such diseases as 
typhoid fever, influenza, diphtheria, plague, etc. They differ from pri- 
mary lobar pneumonia in their etiology, their histological features and 
their clinical course. The same may be said of terminal pneumonias 
which often develop in the last days of chronic exhausting diseases, which 
give only slight and indistinct symptoms and which are very apt to be 
overlooked. 

Complications. — In view of the active pathogenic qualities of the 
pneumococci and of the fact that in most if not all cases of pneumonia 
they are carried to all parts of the body in the circulating blood, it seems 
somewhat strange that serious complications are not more frequent even 
than they are. 

The Lung. — Instead of proceeding to resolution in the usual w^ay a 
part of the hepatized area will occasionally suppurate, break do^m and 
form an abscess, or the blood supply of a certain portion may be cut off 
and gangrene result. On the other hand, the consolidated area instead 
of resolving or breaking down may be the seat of a productive inflam- 
mation with development of new connective tissue, organization of the 
exudate and permanent damage from fibroid induration or cirrhosis. 
These complications are not common. Delayed resolution has already 
been spoken of. Contrary to popular belief, tuberculosis is rarely, if 
ever, engrafted upon a lobar pneumonia. Such apparent instances are 
from the outset really cases of tuberculosis of the acute pneumonic type 
simulating lobar pneumonia. 

The Pleura. — Affections of the pleura are among the most frequent 
and important of complications. A fibrinous inflammation of the pleura 
covering the inflamed lobe is rarely lacking and is hardly to be classed as 
a complication. Pleurisy with effusion develops frequently in the 
latter part of the disease and, usually, so insidiously that frequent and 
careful physical examinations may be needed to demonstrate its presence. 
Empve.ma, thoiiiih less frequent than serous effusion, is by no means 
uiicoiiniion. Tlie ])us usually contains pneumococci in large numbers. 



DISEASES OF THE LUNGS 25 

The Circulatory System. — Next to serous pleurisy and empyema peri- 
carditis is probably the most frequent of the serious complications. It 
is especially apt to develop in double and in left-sided pneumonia and 
is said to be commoner in children than in adults. It may be fibrinous, 
serous or purulent in character. It is sometimes difficult of recognition 
even when repeatedly and carefully sought for. 

Acute endocarditis is also not uncommon. Usually it is of the 
malignant or ulcerative type. It attacks both the right and left side of 
the heart and in the septic thrombi upon the affected valves the diplo- 
coccus pneumonice is usually to be found in pure culture. 

Venous thrombosis and embolism of the cerebral or other arteries 
are rare complications. 

Meningitis is a grave and not very infrequent complication. It is due 
to infection of the meninges by the pneumococcus. Acute arthritis, acute 
nephritis, jaundice, croupous colitis or dysentery, parotitis, otitis media 
and neuritis are occasionally met with. 

Diagnosis. — The disease is usually easily and promptly recognized. 
The chill and rapid rise of temperature, the sharp pain, the cough and 
rusty sputa, the rapid breathing and the characteristic physical signs 
furnish, in typical cases, an unmistakable clinical picture. Even when 
the physical signs are late in developing the other symptoms are usually 
sufficient for a prompt diagnosis. In children and in alcoholic subjects 
the cerebral symptoms may be so pronounced as to mask the true nature 
of the trouble. In debilitated and aged patients, too, the onset may be 
insidious and the rational symptoms slight and indefinite. A careful 
physical examination, however, will usually overcome the difficulty in all 
these cases. In rare instances the pain may be referred to the abdomen 
and may be associated with muscular rigidity. Occasionally such cases 
have been mistaken for appendicitis or gall-bladder disease. Pleurisy 
with effusion and empyema, especially in children, sometimes give phys- 
ical signs which closely simulate those of consolidation. There may be 
loud bronchial breathing and bronchophony and even little or no diminu- 
tion in vocal fremitus. In such cases the exploratory needle may be 
needed to clear up the diagnosis. 

The Blood. — The leukocyte count is regularly increased, often to 
30,000 and sometimes to more than 50,000. Such a leukocytosis, coupled 
with the rational symptoms of pneumonia, makes the diagnosis highly 
probable even in the absence of definite physical signs. 

An equal increase is rarely met with except in cases of active sup- 
puration, or cerebrospinal meningitis. The percentage of polynuclears is 
usually increased. 

Pneumonia may, however, be accompanied by a normal leukocyte 
count or even a leukopenia. With severe constitutional symptoms a 
leukopenia is of unfavorable import. 

Blood cultures may yield the pneumococcus, but usually have negative 
results. 

Pulmonary tuberculosis of the acute i)iieum()nic type is occasionally 



26 



DISEASES OF THE RESPIRATORY TRACT 



marked by so violent an onset and such rapid consolidation as to make 
its differentiation from lobar pneumonia impossible until tubercle bacilli 
or elastic tissue appear in the sputum. In general it may be said that 
errors in diagnosis are best avoided by frequent and painstaking examina- 
tions of the thorax and of the sputum. 

Prognosis. — The mortality of lobar pneumonia varies much at differ- 
ent times and in different locations. In general it ranges between 25 and 
35 per cent. In children the death rate, in contrast to that of broncho- 
pneumonia, is very low. The mortality is highest among those of ad- 
vanced years and those debilitated by alcohol or by chronic disease. The 
extent of lung involvement does not play a prominent part in determining 
the prognosis. Much more important than the extent of consolidation 
are the degree of toxemia and the character of the heart action, and 
these frequently bear no relation to the size of the lesion. The advent 
of pulmonary edema is always of grave significance. Marked abdominal 
distention also adds much to the seriousness of the situation. 

Such complications as meningitis and malignant endocarditis are 
always fatal. 

Treatment. — No satisfactory specific method of treatment is yet 
known, and the best results are still obtained from intelligent and watch- 
ful treatment of the symptoms as they arise. 

The attempts to cut short the disease by venesection or by such drugs 
as veratnim viride or tartar emetic have been altogether abandoned as 
useless if not actually harmful. 

Absolute rest in bed and freedom from all movement or excitement 
must be insisted upon. The room should be cool, quiet and thoroughly 
ventilated and the bed covering and clothing light and comfortable. (See 
Appendix, p. 582.) The diet should be fluid (milk, broths, gruels, etc.), 
should be given in small amounts and at frequent intervals and should 
be carefully watched with a view to the prevention of flatulent distention. 
A calomel purge at the outset is usually desirable. 

In the first days of the disease the distressing pain in the side and 
short, dry cough are the symptoms most apt to demand attention. If 
the pain is not severe it can often be controlled by the use of hot flaxseed 
poultices or of ice-bags applied to the painful area. If the pain is veiy 
severe and is constantly aggravated by the cough, and if the patient is 
restless and sleepless because of it, then morphine should be given sub- 
cutaneously in repeated doses of from Yu to )^ of a grain. The drug 
at this stage can safely be given and is often of the greatest possible 
value in relieving the pain and cough, in producing sleep and thus saving 
the patient's strength. Later in the disease, when dyspnea and cyanosis 
appear, it should be used only with great caution, because of its effect 
up(m the respiratory center. Fortunately it is then not often needed. 
For the cough alone codeine (gr. Ys-Yi) or heroin (gr. }^-Ko) may 
be used. The usual expectorant mixtures have little effect, are apt 
to disturb digestion, and are therefore to be avoided. 

The TEMPERATURE Itself docs not require treatment unless it be unusu- 



DISEASES OF THE LUNGS 



27 



ally high or unless cerebral symptoms be marked. It is best reduced by 
cold packs, alcohol sponge baths or ice-bags to the chest. Tub baths, 
which have been strongly recommended by some, are open to the serious 
objection that they cannot be used without causing the patient much 
disturbance and fatigue. Our best means of combating the toxemia is 
the introduction of large quantities of fluid which, by diluting the toxins 
and causing their increased elimination by the kidneys, tend to diminish 
their noxious effects. This can be done most easily by insisting upon the 
patient 's drinking freely and frequently of water or lemonade. The same 
purpose is accomplished by the use of subcutaneous infusions of normal 
(0.8 per cent.) salt solution (Oss-Oj) or of large enemata of the same 
sort. 

The progressive v^eakening of the heart is the symptom which 
demands most attention. It varies greatly in different cases. Some cases 
require no stimulation whatever and this is especially apt to be true if 
great care has been exercised in guarding the patient's strength in the 
early days, by enjoining absolute rest, relieving pain and cough and in- 
ducing sleep. In a majority of cases the heart, in the later days of the 
disease, will require some support and stimulation. For this purpose 
alcohol is the drug most widely used. It is best administered in the form 
of whiskey or brandy (oss-ji every 2, 3, or 4 hours) well diluted with 
water or in milk. While alcohol seems to be of great value in suitable 
cases, its routine administration in every case cannot be too strongly 
condemned. Nor is it always necessary or wise to give it in alcoholic 
subjects. A stimulant of perhaps greater value than alcohol is strych- 
nine. It is given by mouth or subcutaneously in doses of gr. 1/60-1/20 
every three or four hours. IMuch difference of opinion exists concerning 
the value of digitalis in pneumonia. It has seemed to the writer to be 
sometimes of great value in critical cases when given in full doses. 
Strophanthus and caffeine are also used. Concerning the value of oxygen 
inhalations there is also much conflict of opinion. Where there is much 
dyspnea and cyanosis they should be tried and persisted in if they do not 
add to the patient's distress. 

Pulmonary edema is always an ominous symptom and should be 
promptly met by increased stimulation and by the frequent application 
of dry cups. Meteorism is best relieved by reduction of diet, by frequent 
hot fomentations to the abdomen and by turpentine enemata. (See Ap- 
pendix, p. 582.) 

Serum Treatment. — Although the critical termination of pneumonia 
seems due in all probability to the development in the body of an active 
antitoxin, the use of antitoxic serum obtained from immunized animals 
has thus far been disappointing and has not yet come into general use. 

Prophylaxis. — In view of the infectious nature of the disease it is 
of great importance that the sputum be disinfected and destroyed with 
the same care as in tuberculosis. The general observance of this simple 
precaution would probably do much to reduce the alarming prevalence of 
this disease. 



28 



DISEASES OF THE RESPIRATOKY TRACT 



BRONCHOPNEUMONIA 
(Lobular Pneumonia. Capillary Bronchitis) 

Definition. — An iutiamiiiation of the finer bronchi and the adjacent 
air-vesicles, occurring in scattered areas throughout both lungs. 

Etiology. — Bacterial infection is regarded as the chief cause of 
bronchopneumonia, although no specific organism has been found. Pneu- 
mococci, streptococci, staphylococci, Friedlander 's bacillus, the diphtheria 
bacillus, Pfeiffer's bacillus of influenza, and other organisms are found in 
the att'ected lungs. 

The disease occurs in three different forms. 

1. Primary bronchopneumonia is met with almost wholly in children 
under two years of age. 

2. Secondary bronchopneumonia is a complication of the acute in- 
fectious diseases, especially those in which bronchitis is marked, as 
measles, Avhooping-cough, diphtheria, and influenza, less often in typhoid, 
small-pox and scarlet fever. It also occurs as a teraiinal complication in 
bronchiectasis, emphysema, chronic bronchitis, and tuberculosis, and also 
in chronic nephritis, diabetes and heart disease. 

3. Aspiration or deglutition pneumonia is a variety of bronchopneu- 
monia caused by the entrance of foreign material, such as vomitus, pus, 
blood, necrotic tissue and the like, into the lungs. Thus during anes- 
thesia or in a stuporous or comatose condition vomitus may be aspirated 
into the lungs. In syphilis, tuberculosis, or cancer of the lar^Tix, pus or 
necrotic material may be drawn into the lungs, or in abscesses rupturing 
into the lungs or respiratory tract the bronchi may be filled by pus. 
Doubtless bacteria rather than the foreign materials are harmful. 

Bronchopneumonia is favored by any influence lowering the resist- 
ance of the patient. Infancy and old age are therefore the periods of 
life most affected. In infancy rickets is an important factor, in old age 
any debilitating disease. 

Morbid Anatomy. — Three groups or types represent different stages 
of the inflammatory process. Both lungs are involved in most cases. 
(1) The lungs present the lesions of bronchitis and about many of the 
bronchi there is a narrow zone of deep congestion. ^Microscopically the 
bronchi contain mucopus. the walls of the bronchi and some of the adja- 
cent interstitial tissues are infiltrated with leukocytes, and the contiguous 
air cells contain leukocytes, epithelium, and mucus, rarely fibrin. The 
posterior surface of the lungs under these conditions shows depressed 
deep-blue areas of collapse, due to the obstruction of the terminal bron- 
chioles. By inflation with a blow-pipe thi-ough the bronchi these 
depressed areas can regularly be filled out. 

(2) The second type shows areas of consolidation about the bronchi 
throughout l)()th lungs. This peribronchial consolidation appears on sec- 
tion as circular, deep-red areas surrounding the bronchi, rising above 
the uninflamed parts of th(^ lung, and feeling distinctly firm to the fin- 
gci-s. The bi'onchi are usually filled by plugs of mucopus. Areas of 



DISEASES OF THE LUNGS 



29 



collapse are regularly present. IMicroscopically the process is the same 
as in the first type except that the consolidation extends more or less 
widely about the bronchi. 

(3) The third type is the pseudo-lobar bronchopneumonia, so-called 
because the consolidation involves the greater part of both lower lobes. 
Fibrinous pleurisy often accompanies this extensive consolidation, and 
the process looks very much like lobar pneumonia. The section, however, 
presents a mottled or marbled appearance, owing to the fact that the 
earlier parts of the inflammatory process affecting the bronchi and adja- 
cent alveoli become lighter in color and thus stand out in contrast to the 
more distant peripheral areas of fresh congestion and consolidation. 
Often the branching figures of the bronchi can be plainly made out. 

The distinctive features of bronchopneumonia are that it centers 
about the bronchi, the consolidation extending peripherally from them, 
that the walls of the bronchi and the adjacent interstitial tissue are infil- 
trated with leukocytes, that the exudate shows more epithelium and rela- 
tively fewer leukocytes in the bronchi and air-cells, and that fibrin is less 
abundant. 

Aspiration pneumonia is often marked by suppuration or gangrene 
in the areas of peribronchial consolidation. 

Symptoms. — The primary form begins with a rise of temperature, 
possibly a convulsion, followed by cough, increased frequency of res- 
piration, and prostration. The child is drowsy, vomiting may occur, and 
the bowels are constipated. The physical signs are those of bronchitis. 
The fever and other symptoms persist about one week. The temperature 
often falls by crisis, and it is difficult except for the absence of signs of 
consolidation to distinguish this affection from lobar pneumonia. 

The secondary type develops from acute bronchitis, either itself 
primary or a part of one of the acute infectious diseases. With the onset 
of pneumonia, the temperature rises to 104° or 105°, the pulse becomes 
more rapid, the prostration more marked, the cough more frequent and 
distressing, but there is no change in the physical signs of bronchitis. 
Gradually as the process extends all the symptoms become severer, the 
dyspnea may become extreme, the respirations reaching 80 to 100 in the 
minute in infants or young children, and inspirations often being marked 
by sinking of the suprasternal parts, the epigastrium and the lateral parts 
of the thorax owing to the obstruction of the bronchi by secretion. As 
the asphyxia increases the child becomes more restless, more stuporous, 
cyanosis appears and deepens steadily, and profuse cold sweating occurs. 
After three or four days of the pneumonia, the lungs being generally 
consolidated, the percussion note over the posterioi' parts of the chest 
becomes duller, the respiration is hfirsh and blowing, and the rales, sub- 
crepitant or loose and sonor-ous, are abundant. Frank signs of consoli- 
dation with dulness, bronchial voice and breathing and increase of vocal 
fremitus may be had over limited areas, but are rare. 

In the elderly, bronchopneumonia very closely resembles that of chil- 
dren, except that the temperature is rarely above 102° or 103°, and the 
cyanosis and dyspnea are not so severe. 



30 



DISEASES OF THE RESPIRATORY TRACT 



The temperature curve in bronchopneumonia is very variable, usually 
of distinctly remittent type. In the primary cases the range of fever is. 
moderate, in the secondary type very high temperatures may be recorded. 
(See Fig. 4.) 

Physical Signs. — In the early stages the only pulmonary signs are^ 
those of acute bronchitis, subcrepitant or mucous rales; later the per- 
cussion note is impaired, especially posteriorly; over both lungs there 
are areas of harsh, high-pitched breathing, as well as rales, and in some- 
cases definite areas of dulness, bronchial voice and breathing. 

Course. — In the primary form the duration is short, a week or ten 
days. The secondary bronchopneumonia is more severe, and, if the 
patient lives, more protracted, lasting for several weeks, possibly for 
months. In this form the temperature falls by lysis, the constitutional 
symptoms disappear and the patient is left greatly enfeebled, and, by 
reason of the changes in the walls of the bronchi, not infrequently suffers, 
from chronic bronchitis or bronchiectasis. 



.mi 

PO?R 

106' 
105' 
104' 


/ 


:l 


3 


If- 


s 




7 


g 












'/ 


/ 


%- 


1 




































































1 






I 


\ 1 


1 




1 






! 


1 


1 


102< 

100° 
99< 

98< 
87« 


























































































PULSE 

ESL 











































































































































Fig. 4. — Temperature curve in bronchopneumonia. 

Diagnosis. — The primary type, especially in children, may be con- 
fused with lobar pneumonia. The sudden onset of the latter, the higher 
and more constant temperature, high leukocytosis, definite signs of con- 
solidation, and termination by crisis should differentiate it. From acute 
bronchitis bronchopneumonia is often distinguished only by the higher 
range of fever, greater prostration, longer course, and generally more 
marked severity. Definite areas of pulmonary consolidation would be 
decisive. 

The secondary type of bronchopneumonia is regularly recognized by 
the conditions under which it develops, and in which lobar pneumonia 
is very rarely met. 

From tuberculosis the more protracted cases of bronchopneumonia 
can be differentiated in many cases only by repeated examinations of the 
sputum. Smears of the pharyngeal mucus may be taken in children wha 
will not expectoi-ate. The blood shows a moderate leukocytosis, usually 



DISEASES OF THE LUNGS 



31 



lower than that observed in lobar pneumonia, rarely exceeding 25,000 
except in cases of very extensive consolidation. 

Prognosis. — Bronchopneumonia is always a grave disease. The mor- 
tality is high in infants and the very old. The primary type usually ends 
favorably. The secondary type is the chief cause of the mortality of 
many acute infectious diseases, especially measles, whooping-cough, diph- 
theria and influenza. Few fatal cases of these diseases occur in which 
bronchopneumonia does not play a large part. 

Treatment. — Prophylaxis. Proper treatment of the acute infectious 
diseases of Avhich bronchopneumonia may be a complication will prevent 
many cases. The general condition of children in hospitals and asylums 
has much to do with the frequency and mortality of this type of pneu- 
monia. Improvement, brought about by good food, fresh air, and atten- 
tion to hygiene will diminish both. Cleansing of the mouth by mild 
antiseptic washes is important in all diseases likely to be complicated by 
pneumonia. 

The treatment of cases of primary bronchopneumonia must be car- 
ried out on the same principles as that of lobar pneumonia. Rest in bed, 
a fluid or soft diet, evacuation of the bowels by enema, if necessary, may 
be all that is required for mild cases. All patients should be carefully 
fed with milk, broths, gruels, and soft solids. Water should be given 
freely and fresh air supplied, no matter what the temperature. 

In the severer cases there are two chief indications: to control the 
bronchitis and to support the heart. Careful feeding and fresh air are 
essentials. Medicines have little or no influence on the bronchitis. Light 
poultices of flaxseed meal applied over the whole anterior or posterior 
chest and renewed every two or three hours often give relief to the cough, 
dyspnea and cyanosis. Priessnitz applications, made by dipping a layer 
of flannel in water at 70°-75° F., then wringing it out, applying it to 
the chest and covering it with several layers of dry flannel, may be used 
instead of the poultice. Such applications may be repeated every three 
or four hours. In some cases a jacket of cotton covering the entire chest 
and kept continuously applied is satisfactory. In adults dry cups may 
be used for the sake of counterirritation. Expectorant mixtures of am- 
monium carbonate or chloride and syrup of ipecacuanha are generally 
recommended, but they are nauseating and of doubtful value. For high 
fever and restlessness a tepid sponge bath, the water at a temperature of 
90° to 95°, is the best remedy. Antipyretics of the coal tar class should 
not be used. For the support of the heart stimulants may be called for. 
Whiskey is probably the best of these and may be given freely in milk or 
other liquids. Digitalis may be given by mouth, and strychnine either 
by mouth or hypodermatically. 

When cyanosis results from the accumulation of secretions in the 
bronchi, relief may be had by an emetic dose of ipecac or by alternate 
douching of the chest with hot and cold water to excite coughing and 
deepen respirations. Opium should be given only in emergency to relieve 
pain or distressing cough, as it tends to promote the accumulation of 



32 



DISEASES OF THE RESPIRATORY TRACT 



secretions which should be gotten rid of. Although children do not ex- 
pectorate, the cough expels the secretions from the bronchi into the 
pharynx and they are then swallowed. 

Convalescence from bronchopneumonia is likely to be slow and diffi- 
cult. At this time a change to a milder climate is often the best of 
treatment. 

CHROXIC INTERSTITIAL PXEUMOXIA 
Sclerosis or Cirrhosis of the Lung. Chronic Fibrous Pneumonia 

Definition. — A chronic inflammation of the pulmonary interstitial 
tissue, resulting in increase of fibrous tissue, either local or general. 

Etiology. — Any lesion of the lung, traumatic or inflammatory, may 
be followed by a sclerosis, which may be classified under this heading. 
The sclerosis is usually localized, but may extend throughout the affected 
lobe. The cases of clinical importance regularly follow (1) lobar pneu- 
monia ; (2) bronchopneumonia in rare cases causing disseminated 
sclerosis of the lung; (3) pleurisy; (4) pressure of aneurisms or other 
tumors upon the lung; (5) syphilis-. (6) inhalation of irritating dust 
of coal. iron, or stone. These cases are described later under Pneumo- 
coniosis. 

Morbid Anatomy. — The essential feature is the increased fibrous 
tissue. (1) In the disseminated form the fibrous tissue is thickened and 
increased about the bronchi, or arteries, or in strands running from the 
pleura or interlobular septa. The bronchi are usually dilated and the 
intervening lung emphysematous. (2) The massive form affects one lobe 
or one lung. The pleura is greatly thickened and adherent. The lung or 
lobe is contracted into a shrivelled mass of dense tissue which is firm, gray- 
ish-white, cuts with' i'^sistance and on section shows a dense mass of 
fibrous tissue surrounding bronchi which are chronically inflamed and 
usually dilated, so as to form cavities of some size. The heart is regu- 
larly displaced toward the affected side in these cases, and the right 
ventricle dilated. 

Symptoms. — These are produced not by the sclerosis of the lung 
itself, but by the chronic bronchitis and bronchiectasis resulting from it. 
There are chronic cough, expectoration, and possibly dyspnea. These 
symptoms vary Avith the course of the bronchitis, improving in summer, 
becoming worse in winter. If the bronchiectasis is marked the patients 
have the paroxysmal cough and expectoration characteristic of that affec- 
tion. Hemorrhage from the lungs is not uncommon. Finally the right 
ventricle becomes dilat-ed and the clinical picture is complicated by the 
signs of cardiac failure, increasing dyspnea, cyanosis, and edema. 

Physical Signs. — In the disseminated type the signs are those of 
bronchitis or bronchiectasis. In the massive or lobar type very char- 
acteristic signs are produced by the retraction of the lung. The affected 
side is shrunken and smaller, the intercostal spaces narrowed or oblit- 
erated by ovorlapiung of the ribs. The spine may be curved. The heart 



DISEASES OF THE LUNGS 



33 



is drawn toward the affected side, and the cardiac impulse may be ex- 
tensive and forcible owing to exposure of the heart by the retraction of 
the lung. Expansion may be practically absent. The affected area is dull 
or even flat. On auscultation the rales of the bronchitis or bronchiectasis 
and varied changes in the respiratory murmur may be heard, diminished 
or intensified breathing, amphoric or even cavernous sounds. The vocal 
fremitus is increased or diminished. The heart may give signs of dilata- 
tion and hypertrophy with murmurs. 

Course and Prognosis. — The affection is chronic and incurable, but 
except in extreme cases consistent with many years of life. 

Diagnosis. — The disease can be distinguished from tuberculosis only 
by the absence of tubercle bacilli from the sputum. 

Treatment. — The only treatment is that adapted to the condition of 
the bronchi and the heart. (See pp. 7 and 183.) 

PNEUMOCONIOSIS 

Definition. — A special form of interstitial pneumonia produced by 
the long-continued inhalation of irritating dust, especially that from coal, 
iron, stone, and the like. The disease has received various names, depend- 
ing on the form of dust concerned, such an anthracosis (coal-dust), 
siderosis (iron-dust), chalicosis (stone-dust), kaolinosis (clay-dust), but 
varies little except in the color of the affected lungs. 

Etiology. — The affection is an occupation disease, brought about by 
working for years in the dust-laden atmosphere of mines, or work-shops 
of special character. Coal-mining and the grinding of sharp-edged tools, 
the making of millstones, grain-shovelling and the like are all hazardous 
occupations. Ordinarily dust inhaled is stopped in the nasal chambers, 
or if it reaches the bronchi is checked there by the action of the mucus 
and the ciliated epithelium. Only when these defensive provisions are 
overwhelmed does it pass through the lining o" 'he finer bronchi and the 
alveoli to reach the pulmonary tissue. Thence the dust is carried by 
leukocytes and the lymph-stream (1) to the lymph-nodules about the 
arteries and bronchi; (2) to the interlobular septa; (3) to the bronchial, 
tracheal, and substernal lymph-glands. Wherever the dust is deposited 
in quantity the tissues are correspondingly pigmented. 

Morbid Anatomy. — The lungs regularly are more or less generally 
pigmented; in the case of miners they may be almost coal-black. The 
tracheal, bronchial, and mediastinal glands are likewise pigmented. The 
lungs also present the lesions of chronic bronchitis and emphysema and 
disseminated patches of fibrous tissue, due to chronic interstitial inflam- 
mation. In some cases, the fibroid areas break down and leave cavities of 
various size, full of mucopurulent material containing the dust. 

Symptoms. — After some years of working in the dusty atmosphere 
the patients develop a chronic cough and expectoration (chronic bron- 
chitis). The sputum is pi<4'rnented, black or gray, and nuTcopui'ulent in 
3 



34 



DISEASES OF THE RESPIRATORY TRACT 



character. Later with the development of emphysema the workers suffer 
from dyspnea and possibly cyanosis. 

Physical Signs. — The patients present the signs of chronic bronchitis 
and emphysema, in rare instances, of consolidation with cavities. The 
X-rays show a diffuse even sclerosis of the lung, suggestive but not diag- 
nostic. Small foci not distinguishable from those of tuberculosis regularly 
appear in the plates. (See Fig. 5.) 




"Fig. 5. — Siderosis of the lung in a granite cutter. Compare the diffuse mottling (or mackerel effect) 
of both lungs with the normal left lung shown in Fig. 6. 

Course and Prognosis. — The disease is chronic, lasting for years. 
The duration of life is shortened, in some cases very notably. Few 
grinders of cutlery live beyond forty, and life in the mines is relatively 
short. 

Diagnosis. — The conditions under which the affection develops make 
the diagnosis easy. Tuberculosis must be excluded by the absence of thQ 
constitutional symptoms and failure to find bacilli. 

Treatment. — Ad('(|uate ventilation in mines and working rooms and 
the use of resi)irators diminishes the frequency of the disease. Change of 
occupation is, of course, desirable for those affected. Otherwise the 
trcatmcTit is that of the chronic bronchitis and emphysema. 



DISEASES OF THE LUNGS 



35 



EMPHYSEMA 

Definition. — Pulmonary emphysema is a dilatation of the infundibula 
and alveoli of the lungs, with thinning or atrophy of their walls. Several 
forms are described : 

(1) Compensatory Emphysema. — Whenever any part of the lungs 
is prevented from expanding in inspiration, there occurs a compensatory 
distention of the remaining parts. In some cases the emphysema so 
caused is local, about tuberculous foci for example, usually it is general. 
Thus when one lung is bound down by adhesions or compressed by pleural 
effusions or tumors, there develops a marked distention of the other side. 
With persistence of the condition the walls of the alveoli atrophy and 
the emphysema becomes permanent. Compensatory emphysema occurs 
particularly in tuberculosis, pneumonias, especially unilateral chronic in- 
terstitial, hydrothorax, empyema and the like. 

The affected side of the thorax looks large, and appears to expand 
more fully than normal, both these features being accentuated by the 
limitation of motion and possibly retraction of the lung primarily dis- 
eased. The percussion note is exaggerated, the voice and breathing in- 
tensified, the vocal fremitus increased. With removal of the cause, the 
compensatory emphysema usually disappears. 

(2) Hypertrophic Emphysema. — In this form we have to do with 
a general dilatation of the infundibula and alveoli of both lungs, espe- 
cially their anterior parts. By reason of the increased size of the lungs 
it has also been called the large-lunged emphysema. 

Etiology. — Two factors are said to be operative : 

1. A congenital defect in the elastic tissue of the lung, a condition 
not proven but assumed to exist to explain the fact that the condition 
develops in only a few of those subjected to conditions calculated to 
cause it. Transmission of the disease in families favors this view. 

2. Increased intrapulmonary pressure, especially that caused by hold- 
ing the breath and straining during expiration, such as occurs in 
pertussis, asthma, and other severe coughing, or in blowing musical 
instruments, blowing glass, and the like. 

The disease may develop in childhood, but is commonly seen in adult 
life, and in men rather than women. 

Morbid Anatomy. — The lungs are large and full, frequently cover- 
ing the pericardium and meeting in the mid-line, when the thorax is 
opened. They do not collapse, are light in weight, pale in color, pit upon 
pressure, and in most cases the over-distended air-vesicles can be clearly 
seen on the surface. On section the lesions of chronic bronchitis, and 
possibly of bronchiectasis, are found. Microscopically there is a thinning 
of the alveolar walls and in places many of the air-vesicles fuse into one 
large bulla. When these changes are marked they lead to a considerable 
reduction in the capillary exposure in the walls of the alveoli and in part 
account for the marked cyanosis. The elastic tissue in the alveolar walls 
shows signs of degeneration and in places may have altogether disap- 



36 



DISEASES OF THE RESPIRATORY TRACT 



peared. The bronchi show chronic inflammation and possibly dilatation. 
The heart shows hypertrophy and dilatation, especially on the right side, 
and there may be chronic congestion of the liver, spleen, kidne}-, and 
other viscera as the result of obstruction to the pulmonary circulation. 

Symptoms. — The marked symptoms of emphysema are cough, dys- 
pnea, and cyanosis. (1) The cough is due to the associated chronic bron- 
chitis or bronchiectasis, and as in those conditions it is regularly better 
in summer than winter, and all the symptoms are greatly aggravated by 
fresh attacks of bronchitis. The expectoration is mucopurulent in char- 
acter, and may be either scanty or abundant. (2) The dyspnea is due 
largely to the failing elasticity of the lung and is therefore mainly ex- 
piratory, resembling that of asthma, Avith which emphj'sema is frequently 
associated. The dyspnea at first is slight, and occurs only on exertion, 
increases gradually, becomes persistent and severe in the advanced stages. 
Inspiration is then short and jerky, expiration prolonged and difficult 
and accompanied with much wheezing. (3) Cyanosis in the early stages 
is slight and transitory, later it becomes constant and very marked. 
Emphysema is one of the few conditions in which, with deep cyanosis of 
the lips, face and extremities, the patient can still go about with com- 
parative comfort. Congenital heart disease or poisoning with one of 
the coal-tar preparations may present a like picture. With advanced 
emphysema the patient usually ajjpears thin, though muscular. In the 
final stages the right heart fails and symptoms of broken compensation 
are present. Hemoptysis is not infrequent in the course of the disease. 

Physical Signs. — The chest is deepened antero-posteriorly, giving it 
the barrel shape; the shoulders are round; the curve of the spine in- 
creased, the clavicles prominent, the anterior chest bulging, the supra- 
clavicular fossas marked. The costal cartilages are rigid and in inspira- 
tion the thorax rises rigidly like a cuirass. On percussion the note is 
exaggerated, or drum-like. The area of pulmonary resonance is increased, 
so that the cardiac dulness is diminished or obliterated, and the lower 
limits of lung resonance are found at the sixth or seventh rib in front and 
the eleventh or twelfth behind. Liver dulness is correspondingly lowered 
and splenic dulness usually absent. On auscultation the inspiratory mur- 
mur is short and weak, expiration is prolonged and high-pitched. Usually 
there are abundant sibilant, sonorous, or mucous rales from the bronchitis, 
especially posteriorly. Dilatation of the right heart may be shown by 
marked epigastric pulsation, pulsation of the veins of the neck, and dilata- 
tion of the superficial veins. 

Diagnosis. — The physical signs are characteristic of emphysema, and 
cannot well be mistaken. 

Course and Prognosis. — The disease is progressive, but slow; and 
under fav(»i-al)lo conditions life may be prolonged for many years. The 
])atients succumb to failure of the right heart or to bronchitis and 
l)r()iH'h()])neumonia. 

Treatment.- -For tlio emphysema, littU^ can be done directly. The 
ell id' indications lie in the trcnitment of the chi'onic bronchitis and avoid- 



DISEASES OF THE LUNGS 



37 



ance of fresh attacks. For these ends a mild, dry climate, such as that 
of Southern California, the Riviera, or Egypt, is desirable during the 
winter months. Attention must be given to the diet and clothing and 
the general health of the patient. With exacerbations of the bronchitis 
the patient must be put to bed and treated as for acute bronchitis. For 
extreme cyanosis and dyspnea arising under these conditions, venesection 
is indicated. Withdrawal of a pint of blood from the arm may save the 
patient when all other measures fail. The efficacy of this measure lies in 
the relief afforded the overburdened right heart. 

ATROPHIC EMPHYSEMA 

Senile or small-lunged emphj^sema is properly an atrophy of the lung^ 
occurring as part of the general atroph}^ of the tissues in old age. The 
chest is small, and the ribs more oblique than normal. The lungs are 
small and collapse on exposure. The intervesicular septa are at^*ophied 
and many alveoli fused into large bullae. Atrophy of the capillaries in 
the septa naturally accompanies the process. The patients suffer from 
winter cough with more or less dyspnea for many years. 

ACUTE VESICULAR EMPHYSEMA 

Under certain conditions of dyspnea marked by strong inspiratory 
efforts, and possibly obstruction of the bronchi, the lungs may be acutely 
distended and remain so for some time. This condition gives some of the 
physical signs of emphysema, enlarged areas of pulmonary resonance, 
an exaggerated percussion note, and many sibilant or sonorous rales 
with prolonged expiration, but there is no atrophy of the elastic tissue 
and no permanent emphysema. The condition may develop rapidly in 
certain cases of bronchopneumonia, cardiac dyspnea, or angina pectoris. 

INTERSTITIAL EMPHYSEMA 

This form of emphysema is produced by rupture of air-vesicles of 
the lungs during strong expiratory efforts, such as occur in whooping- 
cough, bronchopneumonia, parturition, or heavy lifting. Postmortem 
the air is found in large blebs in the interstitial tissue and beneath the 
pleura, especially at the roots of the lungs or along their anterior margins. 
Rupture through the pleura may cause pneumothorax, or in some cases 
the air makes its way through the mediastinum into the neck or even 
the arms, appearing as subcutaneous emphysema of these parts. 

ABSCESS OF THE LUNG 

Etiology. — Abscess of the lung is never primary but may result from 
several conditions. 

1. Infected wounds such as those produced by broken ribs or by 
bullets. 

2. Abscesses in neighboring organs, the liver, the niediastinum. the 



38 



DISEASES OF THE RESPIRATORY TRACT 



pleura, or the peritoneum, may by extension produce suppuration in the 
lung, or may rupture through it. 

3. Inliammatory processes in the lung may terminate in suppuration, 
(a) Lobar pneumonia frequently results in an abscess occupying more 
or less of a lobe, (b) Bronchopneumonia, especially the aspiration pneu- 
monia produced by the inspiration of septic material of any kind, gives 
rise to one or more abscesses of smaller size, (c) Tuberculosis in its 
advanced stages may produce large abscesses of the lung. 

4. ^Multiple metastatic abscesses of the lungs are frequently met with 
in pyemia of all forms, in malignant endocarditis, and the like. 

5. Xew growths of the lung are often complicated by suppuration and 
abscess formation either in the area of the growth or adjacent parts. 

Morbid Anatomy. — The multiple abscesses of pyemia, or aspiration 
pneumonia, are numerous and of small size. The abscesses fol- 
lowing lobar pneumonia, or infected wounds, or produced by extension, 
are usually single and may involve the greater part of a lobe or a lung. 
Tuberculous abscesses or cavities may be of am^ size or number. The 
contents of the abscess are pus, usually greenish-gray in color, and foul- 
smelling, but not so oifensive as in gangrene or putrid bronchitis. Elastic 
tissue from the broken-down lung may be found in it. Bacteria of various 
kinds may be present. In the pus discharged from abscess of the liver 
the ameba has been found. 

Abscesses of the lung are regularly complicated by pleurisy, which 
may be purulent, or the abscess may rupture through the pleura and 
thus give rise to empyema. Most often the abscesses rupture into a 
bronchus and the pus is discharged in this way. 

Symptoms. — The multiple abscesses of pyemia give no distinctive 
symptoms and are usually not recognized during life. In other cases the 
patients present fever, continuous or of remittent type, sweating, rapid 
pulse, cough, dyspnea, and pain in the chest. These s^Tuptoms are en- 
grafted on those of the original condition, such as bronchopneumonia or 
lobar pneumonia. Sooner or later the pus is expectorated. Often the 
abscess ruptures suddenly and the patient coughs up a large quantity of 
foul pus at once. A leukocytosis is present except in tuberculous cases. 
The secondary anemia is usually marked. 

The PHYSICAL siGxs are those of a localized collection of fluid or, 
after the rupture of the abscess, of cavities. Thus after lobar pneumonia 
dulness persists, usually with a gradual loss of the intense bronchial voice 
and breathing and vocal fremitus. If the abscess is large and close to 
the pleura the signs may be those of empyema, and only the depth at 
which the pus is found on exploration or operation locates the process as 
pulmonary. In the bronchopneumonic cases the abscesses are smaller and 
much more difficult to locate. 

Course and Prognosis. — The course is usually very protracted, 
^laiiy of the cases are fatal. If the abscess discharges through a bronchus 
or is drained, recovery may take place by gradual obliteration of the 
cavity, usually requiring many months. 



DISEASES OF THE LUNGS 



39 



Diagnosis. — This is often not made except at autopsy. In some cases 
the combination of the constitutional symptoms of suppuration and the 
expectoration of large amounts of pus make the diagnosis easy. The 
demonstration of elastic tissue in the pus is proof of destruction of the 
lung. Practically the cases of greatest difficulty are those following 
lobar pneumonia, where the persistent fever and physical signs suggest 
delayed resolution, abscess of the lung, or empyema, or tuberculosis. In 
these cases repeated exploration of the chest with a large calibered 




Fig. 6. — An abscess of the lung occupying most of the left chest, obscuring the cardiac outlines and 
darkening the whole area of the left lung. 

needle is essential. At times only the depth at which the pus is found 
indicates its location in the lung. Occasionally the sudden discharge of 
pus through a bronchus clears up the diagnosis. The blood in these cases 
regularly shows a leukocytosis usually accompanied by an increase in the 
percentage of polynuclears. 

The X-rays show a heavy shadow on the affected side, rarely sharply 
defined, and not distinguishable by these means alone from pleural effu- 
sions, thickening of the pleura, or consolidation of the lung. (See 
Fig. 6.) 

Treatment. — Careful feeding and nursing help to maintain the 
patient's strength. No medicinal treatment is known to affect the process 



40 



DISEASES OF THE RESPIRATOKY TRACT 



in the lung. When an abscess is discharging postural treatment may be 
of value, the patient lying tlat upon the bed with the foot raised, or upon 
one side or the other, as is found to best drain the abscess, for some hours 
each morning, until the cavity is emptied of its contents. He may then 
be allowed to assume an ordinary position. When an abscess is located 
by the exploring needle, drainage by surgical intervention is required. 
In some cases where the abscess is being imperfectly emptied through a 
bronchus, operation may be necessary. 

GANGRENE OF THE LUNG 

Etiology. — Gangrene of the lung is never primary, but complicates 
some previous affection of the lung, bronchitis, bronchopneumonia, lobar 
pneumonia, or abscess, or embolism of the pulmonary artery. Why gan- 
grene develops in some cases and not in others is not known. Lowered 
tissue resistance is the most plausible suggestion. Gangrene of the lung 
is relatively rare, but is most often seen following (1) aspiration broncho- 
pneumonia or the bronchopneumonia complicating noma; (2) bronchi- 
ectatic or tuberculous cavities; (3) lobar pneumonia; (4) embolism of 
the pulmonary artery, when the embolus has come from a gangrenous 
focus; (5) in debilitating diseases, such as typhoid fever, diabetes, and 
the like. 

Morbid Anatomy. — The gangrenous area of the lung may be large 
or small, single or multiple. As usually seen the affected portion presents 
a central cavity containing a dark, putrid fluid, its walls composed of 
soft, ragged, greenish-black material, bej^ond which is a more or less 
extensive area of pneumonic consolidation. Pleurisj^ or empyema is asso- 
ciated, sometimes pyopneumothorax. Abscess of the brain is not infre- 
quently found as a complication. 

Symptoms. — The inception of gangrene is preceded by the symptoms 
of the primary affection of the lung. The development of gangrene is 
marked by an increase in severity of the general symptoms and the ap- 
pearance of the characteristic sputum. The expectoration and breath are 
intensely fetid, such as are met with in no other condition except putrid 
bronchitis. The expectoration is abundant, as a rule, and the patient is 
harassed by a constant cough, as w^ell as the frightful taste and odor 
of the secretion. In children with noma, the expectoration being absent, 
and the breath already contaminated by the condition of the mouth, there 
is no conclusive evidence of gangrene of the lung, yet it is often present. 
The constitutional symptoms usually become those of intense sepsis and 
the patients promptly succumb. In some cases, however, the course is 
less acute and recovery is possible. 

Physical Signs. — These are those of the underlying pulmonary con- 
diti(m, bronchitis, pneumonia, or infarction. In advanced cases cavities 
may be made out. 

Diagnosis. — This must be based on the odor of the breath and sputum, 
and tlic cliaracter of tlie latter. If collected in a glass, the sputum sep- 



DISEASES OF THE LUNGS 



41 



arates into three layers, the lowest of greenish-black granular material, 
the middle a thin dirty fluid, and the top of thick, dark, frothy mucus. 
Microscopically it shows granular material, fatty crystals, quantities of 
bacteria, and usually elastic tissue. 

Treatment. — This, as in abscess of the lung, must be mainly sup- 
portive. Sprays or inhalations of carbolic acid, creosote, and the like, 
may be used to mitigate the odor. A few cases of successful drainage of 
gangrenous areas in the lung have been recorded. 

NEW GROWTHS OF THE LUNG 

Benign tumors of the lung are exceedingly rare. Adenoma, fibroma, 
chondroma, and osteoma are possibilities. Malignant tumors occur as 
carcinoma or sarcoma. Primary new growths of this class are exceedingly 
rare. 



Fig. 7. — An intrathoracic growth giving an extensive shadow above and to the right of the heart. 
The growth gave no physical signs, but produced attacks of dyspnea closely resembling bronchial 
asthma. It was probably a sarcoma of the mediastinal nodes and lung. 

Carcinoma occurs secondarily to primary growths in the breast, glands, 
esophagus, or stomach, or other viscera. Sarcoma most often follows sar- 
coma of bone, but the primary growth may be in any part. Carcinoma 
is rarely met with under 40. Sarcoma may occur at an earlier age. 

Morbid Anatomy.- — The new growths are single or multiple masses 



42 



DISEASES OF THE RESPIRATORY TRACT 



of varying size, whitish or gray in color, compressing the lung or adjacent 
structures in their growth, frequently involving the pleura and the chest 
wall. 

Symptoms. — An interval of months or years following the primary 
growth may elapse before the lung is involved. The symptoms are slowly 
developed. These are thoracic pain, cough, increasing dyspnea, possibly 
hemoptysis, and eventually cachexia. The symptoms grow progressively 
worse. Life is rarely prolonged over 6 or 8 months after evidence of 
pulmonary involvement. 

The physical signs are uncertain. A localized area of dulness vrith 
diminished voice and breath sounds may be made out. Pleurisy with 
hemorrhagic effusion is common. In the pleural fluid cells with mitotic 
figures may be found. A radiogram may be very helpful in deciding 
the diagnosis. (See Fig. 7.) 

Treatment is purely palliative. ]\Iorphine may be given to relieve 
pain and distress. 

DISEASES OF THE PLEURAE 

ACUTE PLEURISY 

For purposes of description acute pleurisy is classified according to 
the character of the exudate as fibrinous or dry, serous or purulent. 
There are no strict lines of division between these forms. Fibrinous 
pleurisy may become serous or even purulent. For the most part the 
etiology of these forms is the same. Whether in any given case of pleurisy 
the exudate shall be fibrinous, serous or purulent, seems to depend in 
large measure upon the general condition of the patient at the time. We 
separate them only for convenience of description. 

Etiology. — (1) Primary: Pleurisy arises at times without apparent 
cause. A certain number of these cases are regarded as rheumatic mani- 
festations. Exposure to cold or wet is usually given as the cause, but the 
more these cases are followed, the greater the number found to be due 
to bacterial infection, especially to the tubercle bacillus. (2) Secondary 
to disease of the lung, pneumonia, tuberculosis, cancer, abscess, gangrene, 
or infarction. (3) Secondary to disease of adjacent organs, the peri- 
cardium, peritoneum, mediastinal glands, or esophagus, the vertebrae, 
ribs, or sternum. (4) Secondary to acute infectious diseases, especially 
rheumatic fever, or to chronic nephritis, gout, or diabetes. 

Bacteriology. — The possibility of pleurisy being due to other causes 
than bacterial infection must be admitted, but in the great majority of 
cases where investigation of the question is possible bacteria are found. 
The tubercle bacillus, pneumococcus, and streptococcus are by all means 
the most common of these, but a number of others, the staphylococcus 
pyogenes, streptococcus capsulatus, Friedlander's bacillus, influenza 
bacilhis, the typhoid bacillus, and many others have at times been found, 
either alone or in association. Any of these organisms may cause a dry, 
serous, or purulent effusion. 



DISEASES OF THE PLEURA 



43 



Fibrinous pleurisy, however, most often yields the pneumococcus or 
streptococcus, the serous effusion the tubercle bacillus, and the purulent 
effusions the pneumococcus or streptococcus. The demonstration of the 
tubercle bacillus often requires the inoculation of the suspected fluid into 
a susceptible animal such as the guinea-pig. 

FIBRINOUS OR DRY PLEURISY 

Morbid Anatomy. — The pleura is lustreless, opaque, granular on the 
surface, and slightly swollen or covered with a more or less thick layer of 
fibrin. Both layers are involved. Microscopically the pleura shows the 
usual changes of acute inflammation. Following such a pleurisy the 
membrane is left thickened and more or less adherent. 

Symptoms. — Pain in the side, especially on deep respiration, or 
motion, cough wdth a slight mucous expectoration or entirely dry, and 
some increase in respiration, possibly dyspnea, mark the onset of dry 
pleurisy. Fever is often absent, but the temperature may rise to 100°- 
101°. The pulse is not rapid and the constitutional disturbance is slight. 

Physical Signs. — The characteristic sign is a dry friction rub, caused 
by the play of the roughened layers of pleura one upon the other, heard 
during both inspiration and expiration, and seemingly close to the sur- 
face. In some cases crepitant or subcrepitant rales only are heard, and 
these are with difficulty distinguished from like rales arising within the 
lungs. 

Course and Prognosis. — The primary cases last but a few days and 
the patients recover within a week. That at least one-third of these cases 
give tuberculin reactions and that 5 or 10 per cent, of them will later 
develop tuberculosis must be remembered. The course of the secondary 
cases will depend upon the underlying cause. The blood shows a mod- 
erate leukocytosis (10,000-15,000) in most cases. 

Treatment. — Limitation of the motion of the affected side by a tight 
bandage or by strapping with adhesive plaster usually relieves the pain. 
Instead an ice-bag or a hot poultice may be used. In some cases the 
severity of the pain requires the administration of codeia or morphine. 
In convalescence the possibility of later tuberculosis must be remembered. 

SEROUS PLEURISY 
(Pleurisy with Effusion) 

Etiology. — Pleurisy with serous effusion may arise from any of the 
causes already cited. It is especially common as an apparently primary 
process, but more than 50 per cent, of these cases can be proven to be 
tuberculous, and at least 30 per cent, of the patients go on to develop 
other evidences of tuberculosis. 

Morbid Anatomy. — The pleura itself has the appearances described 
for the fibrinous form. In addition there is present a more or less abun- 
dant exudate of serum. This is regularly a clear yellowish fluid with floe- 



44 



DISEASES OF THE RESPIRATOEY TRACT 



culi of fibrin, all^aline to litmus, having a specific gravity of 1015 or over, 
and containing considerable quantities of albumin. Microscopically the 
fiuid shows fibrin, leukocytes, both polynuclear and mononuclear, and 
endothelial cells. The lung is more or less compressed by the effusion 
and may be reduced to an airless mass occupying only the upper and 
posterior part of the thorax. With large effusions, the heart may be 
displaced to the opposite side, the diaphragm and liver or spleen 
depressed. 

Symptoms. — The onset is usually insidious, but may be abrupt. The 
disease may begin with a sudden fever, possibly a chill, cough, dyspnea, 
and pain in the side suggesting a pneumonia. On the other hand, the 
onset is often so gradual that large quantities of fluid have collected 
before the patient comes under observation. The chief symptoms are 
then (1) fever of moderate degree, rarely exceeding 103°, remittent in 
type and lasting from one to three weeks (see Fig. 8) ; (2) marked pros- 




FiG. 8. — Temperature of pleurisy with effusion. 



tration with moderate increase in the pulse ; (3) a cough with mucous ex- 
pectoration ; (4) dyspnea varying Avith the quantity of the effusion, very 
slight and appearing only on exertion in mild cases, so severe as to re~ 
quire the upright position (orthopnea) and associated Avith cyanosis when 
the effusion is large; (5) pain in the side is usually present at the onset, 
disappears with the accumulation of the fluid, and returns upon its 
subsidence. 

Physical Signs. — These must vary Avith the amount of the effusion. 
With small effusions the signs are limited to a slight diminution in the 
respiratory expansion of the affected side, with dulness over the fluid, 
usually at one base behind, and diminution in the voice, breathing, and 
vocal fremitus over the same area. Otherwise the examination may be 
negative. With large effusions very striking physical signs may be 
developed. 

Inspection. — The affected side of the chest is nearly immobile, the 
only motion appearing at the apex in front. It looks larger than the 



DISEASES OF THE PLEUR.E 



45 



other and a difference of 1-2.5 cm. may be found on measurement. The 
lower intercostal spaces behind and in the axilla may bulge. The apex 
beat may be displaced toward the opposite side. 

Palpation confirms the immobility of the chest, the prominence of 
intercostal spaces, and the displacement of the apex beat. The vocal 
fremitus is diminished or lost below the level of the fluid. The transition 
is not sharply marked. 

Percussion. — Below the level of the fluid there is dulness, increasing 
to flatness at the base in the case of large effusions. Above the fluid in 
the back the note is still dull from compression of the lung. In front it 
is normal, or dull, or tympanitic. A dull tympanitic note obtained on 
percussion beneath the clavicle or lower anteriorly is spoken of as Skoda 's 




Fig. 9. — The line of dulness in pleurisy, with effusion sloping downward and forward parallel to the ribs. 

resonance. The tympanitic note normally obtained on percussion of the 
area between liver and spleen (Traube's semilunar space) may be oblit- 
erated. The line of dulness marking the upper level of the fluid is not 
horizontal but curved with its highest point usually in the axilla, falling 
gradually tow^ard both spine and sternum, the forward end usually being 
the lower. This line is commonly described as the S-shaped line of dulness 
of Ellis, but it has a single not a double curve. (See Fig. 9.) 

Percussion on the sound side frequently discloses a triangular area 
of dulness adjacent to the vertebral column, the apex of which is at a 
point on the spine corresponding to the level of the fluid in the other 
chest, the base of it on the line of the lower level of the pleura, the length 
of the base line varying from 1 to 3 inches. This area of dulness on 
the sound side (Grocco's paravertebral triangle, see Fig. 10) is attributed 
to the distention in that direction of the pleural sac containing fluid, 



46 



DISEASES OF THE RESPIRATORY TRACT 



and it is claimed that the height of the triangle is an indication of the 
level of the fluid. The sign is not always to be elicited. 

Auscultation. — Below the level of fluid the respiratory and voice 
sounds are usually diminished or lost, above the level they are preserved, 
and may be normal, diminished, or accentuated. Some notable variations 
are met with. At times the voice and breathing below the level of the 
fluid ma}^ be definitely bronchial in character, very suggestive of the signs 
of pneumonia, although nearly always more distant and feeble than in 




Fig. 10. — Pleurisy with effusion on the left side. Grocco's triangle on the right. 

pneumonia. Near the level of the fluid the voice often has a curiously 
nasal twang, to which the name of egophony has been very inappro- 
priately given. 

Above the fluid pleural friction rubs or rales may be obtained, and 
there is no doubt that similar signs are sometimes obtained through fluid, 
although this should theoreticallv be impossible. 

The sound lung often develops a compensatory emphysema, appears 
distended, and gives an exaggerated pulmonary resonance on percussion 
with corresponding changes of voice and breathing. With the absorption 
or removal of the Huid the dulness on the affected side diminishes, but 
does not entirely dis;i|)])(^ar for weeks or months. At this time the coarse 
friction nd) or rales of dry pleurisy may be heard. Limited expansion on 
the affected side and diminution of voice and breathing sounds, as well 
as the dulness, may persist long after the patient is apparently well. 



DISEASES OF THE PLEURA 



47 



Course. — Many of the cases terminate promptly within two weeks; 
others are protracted for many weeks or months. The tuberculous cases 
are usually longer, and in some instances the patients go on to develop 
the signs and symptoms of pulmonary tuberculosis. 

Prognosis. — Death in pleurisy with effusion is unusual, but does 
occur. It is particularly likely to follow some sudden change of position 
or the removal of the fluid. 

Diagnosis. — In the mild cases unattended by pulmonary symptoms 
pleurisy with effusion may be easily overlooked. With definite physical 
signs hydrothorax, empyema, lobar pneumonia, or the thickened pleura 
and adherent lung of previous pulmonary affection must be distinguished. 

Hydrothorax is usually recognized by the conditions under which 
it occurs, as part of a general anasarca due to heart, kidney, or other 
disease, and by the absence of fever. The fluid in hydrothorax regularly 
shows a specific gravity below 1015, a less amount of albumin, and a cellu- 
lar content chiefiy of endothelial cells. 

Pneumonia is distinguished by the sudden onset with the initial chill, 
higher fever, greater prostration, the flushing of the face, the greater 
restlessness and distress, the more profuse and sometimes blood-tinged 
expectoration. The bronchial voice and breathing of lobar pneumonia 
are usually louder and closer to the ear than in pleurisy with effusion 
and the vocal fremitus in the latter is diminished or lost. The leukocyte 
count in pleurisy with effusion is rarely above 15,000, in pneumonia it is 
comjQonly above. Finally in some cases the exploring needle is required 
to determine the presence or absence of fluid. 

Empyema is most often a sequel of pneumonia. The fever is higher, 
sweating more marked, prostration and emaciation more profound. The 
physical signs are practically the same, except that displacement of the 
heart is more likely to be marked in empyema. Empyema will regularly 
show a leukocytosis above 15,000, often with an increased polymorpho- 
nuclear percentage. The exploring needle is regularly required to com- 
plete the differentiation. 

The absence of constitutional symptoms usually enables us to recog- 
nize the conditions resulting from previous pulmonary disease, such as 
a thickened pleura with adhesions, but in other cases exploration may be 
required. Radiographic examination of the thorax may be of value. 

The BLOOD in pleurisy with effusion shows in most cases a leukocytosis 
between 10,000 and 15,000, very rarely above the latter figure. Often 
there is no leukocytosis, and in the tuberculous eases there may be a leuko- 
penia. The latter cases may also show a differential lymphocytosis. A 
moderate secondary anemia is regularly present. 

Pleural Fluid. — The exudate in pleurisy with effusion is ordinarily 
a clear yellowish serum, alkaline to litmus, of a specific gravity of 1015 
or higher, and containing much albumin. The fluid may contain flakes 
of fibrin, may coagulate spontaneously, and is frequently tinged with 
blood drawn either from the pleura or lung by the needle. Effusions 
which are permanently bloody are always highly suggestive of tuberculous 



48 



DISEASES OF THE RESPIRATORY TRACT 



or cancerous processes. The cytology, that is, the differential counting 
of the cells to be found in the exudate, is sometimes of help in diagnosis. 
Widal's formulae are as follows: — (1) a predominance of pol^^nuclear 
leukocytes means an effusion of infectious origin (pneumococcus, strepto- 
coccus, staphylococcus) ; (2) of lymphocytes, a tuberculous effusion; (3) 
of endothelial cells, especially in plaques or sheets, of mechanical origin 
(hydrothorax) . In cancer, cells with mitotic figures in the nuclei or of 
such unusual character as to. suggest malignant growth may be found. 




Fig. 11. — The aspiration instruments — needle, tubing, bottle and syringe. The second tip on the 
syringe should be removed. The scale on the bottle indicates the number of ounces of fluid required 
to reach tne several levels. 

The bacteriology of the fluid is also important. The usual pyogenic 
bacteria may be sought in smears and cultures. Tubercle bacilli, although 
present, may be demonstrable with difficulty. If the fluid clots they 
should be sought in smears from the clot, or the clot may be digested and 
smears made from the resulting sediment (method of inoscopy). Finally 
intraperitoneal inoculation of guinea-pigs with doses of from 10 to 50 ce. 
of the pleural fluid is most conclusive, but requires from four to six weeks 
for a decision. 

Treatment. — In the early stages the treatment is that of dry pleurisy. 
AVith the appearance of fluid the patient should be put to bed, and a dry 
diet presc]'i])ed. Efforts to control the effusion l)y the administration of 



DISEASES OF THE PLEURA 



49 



saline cathartics, by sweating, and counterirritation by mustard, turpen- 
tine or iodine are regularly made, but are rarely of value. The salt-free 
diet may be tried. Careful feeding and nursing are most important. 
Aspiration of the fluid must be practiced (1) if dyspnea develops from 
the presence of the fluid; (2) if the effusion rises above the mid-scapula, 
whether or no dyspnea be present; (3) if after a week or ten days the 
fluid shows no signs of absorption ; (4) if, after removal, the fluid returns, 
aspiration is to be repeated as often as necessary. (See Figs. 11 and 12.) 

Technique of Paracentesis. — The operation may be done with the 
patient lying upon one side or, better, sitting upright. The principles of 
asepsis must be observed as to the preparation of the patient's back and 
the operator's hands. The instruments to be used, commonly the 




Fig. 12. — Aspiration of the chest. The curved line on the patient's back marks the position of the 
scapula. The needle is inserted in the 8th intercostal space. 

Dieulafoy or Potain aspirator, should be sterilized. The apparatus should 
then be tested to see that it is working properly, and in its use the fact 
should never be forgotten that it is quite possible with the apparatus 
as made to charge the bottle with compressed air instead of evacuating it. 
The site of aspiration must depend upon the location of the signs of fluid ; 
usually the seventh or eighth intercostal space below the angle of the 
scapula is selected. The puncture may also be made in the sixth space 
in mid-axilla. The fluid should be allowed to flow off slowly, and the 
aspiration promptly stopped if the patient shows signs of dyspnea or dis- 
tress from the removal. In dealing with lai-go effusions it is wisest not 
to draw off more than one litre at a time, though som(' cliniciaus advocate 
tlie removal of all th(^ fluid j)()ssil)le at any time. The ()))orati()n is i-arely 
attended by bad results. Severe pain and some bleeding is regularly 
4 



50 



DISEASES OF THE RESPIRATORY TRACT 



caused by contact of the lung with the sharp needle, as the fluid subsides. 
Hemoptj^sis is not uncommon. Pneumothorax often results from puncture 
of the lung. Subcutaneous emphysema may also develop. Severe dys- 
pnea, edema of the lungs, sometimes accompanied by an albuminous ex- 
pectoration, may result. Sudden death has occurred in some cases. The 
advantages of the operation far outweigh its dangers. It should be used 
and repeated as necessary. A preliminary injection of morphine gr. 14 
and atropine gr. 1-100 appears to prevent the distress and possibly col- 
lapse which sometimes follow the operation. 

In convalescence every effort should be made to restore the vigor of 
the patient, and in many cases the patients should be treated as for 
incipient tuberculosis. 

PURULENT PLEURISY 
(Empyema) 

Etiology. — The general etiology of pleurisy has already been given. 
The purulent exudates naturally occur most often as complications of 
processes alread.y septic: (1) infected wounds; (2) abscesses or suppura- 
tive processes extending from the lung, the thorax, pericardium, peri- 
toneum or other adjacent structures; (3) acute infectious diseases, most 
of all lobar pneumonia. The pleural effusions complicating or following 
lobar pneumonia are nearly always purulent, and the majority of cases 
of empyema are seen in that relation. It may follow other infectious dis- 
eases, especially scarlet fever or typhoid. (4) Any pleurisy with effusion 
may develop into an empyema. Such transformation may rarely be 
attributed to infection due to aspiration. In most cases it is a natural 
evolution. 

Morbid Anatomy. — The fluid in empyema may vary from slightly 
turbid serum to thick pus. The odor is sometimes very disagreeable. The 
pleura is thickened and covered with a dense layer of fibrin. Adhesions 
are common and the effusions are frequently encysted. The lung is com- 
pressed and the conditions are as in pleurisj^ with effusion, with possibly 
greater displacement of the adjacent viscera. The primary focus may be 
found in the lungs, the thorax, or some of the adjacent viscera. 

Bacteriology . — Empyema is most often caused by the streptococcus. 
The pneumococcus is not uncommon, and the staphylococcus is occasion- 
ally found. Tubercular empyema is sterile to cultural methods. 

Symptoms. — The manner of onset and symptoms cannot be distin- 
guished from those of pleurisy with effusion, except that when suppura- 
tion is well established and the amount of pus large, the temperature is 
usually higher, more remittent in type, accompanied by more profuse 
sweating and more rapidly developing anemia and emaciation. In severe 
cases there may be repeated chills, profound sepsis, and rapid exhaustion. 

Physical Signs. — All the signs enumerated under pleurisy with effu- 
sion are found in this condition. Certain signs are usually more marked. 
(1) The enlargement of the affected chest is greater. (2) The displace- 



DISEASES OF THE PLEURA 



51 



ment of the heart is more marked. (3) The whispered voice, sometimes 
heard over clear fluid, is not transmitted (Bacelli's sign). (4) In very 
rare cases affecting the left side a pulsation synchronous with the heart 
beats is detected (pulsating pleurisy). (5) The chest walls may become 
edematous. (6) In rare instances an empyema may rupture through 
the chest walls, leaving a discharging sinus. 

Course. — Empyema, unless relieved by operation, regularly results 
fatally. Spontaneous cure is possible, either by rupture of the pus into 
a bronchus and discharge of it through the mouth or through breaking 
down of the chest wall (empyema necessitatis, see Fig. 13). In either 
event recovery is long delayed and the outcome doubtful. The possibility 




Fig. 13. — An empyema of the left pleura presenting externally empyema necessitatis. 

of the absorption of encysted collections of pus in the pleura must be 
admitted. In the great majority of cases the conditions become steadily 
worse until the patient is relieved by operation or dies. 

Prognosis. — Pneumococcus infections are mildest and as a rule run 
a favorable course. Streptococcus infections are likely to be most acute 
and most severe. The tubercle bacillus usually produces an insidious 
infection which has a strong tendency to become chronic, is very difficult 
to overcome, and is likely to be complicated by pulmonary or other 
tuberculosis. 

Diagnosis. — The differential diagnosis is essentially that of pleurisy 
with effusion, except that in empyema there is usually a leukocytosis and 
an increase in the polynuclear percentage. This brings the clinical pic- 
ture into close relation to that of pneumonia. The differentiation should 



52 DISEASES OF THE RESPIRATORY TRACT 



always be finally determined by the exploring needle. No other test is 
dependable. 

Treatment. — In the early stages these cases must be treated like 
fibrinous or serous pleurisy. When the presence of pus is determined, 
drainage by surgical procedure is essential. In young children simple 
incision in an intercostal space and the insertion of a drainage tube are 
sometimes suffieient, but in most cases the resection of a rib is necessary 
to secure adequate drainage. In very chronic cases the resection of a 
number of ribs may be necessary. Cases of recovery after aspiration of 
an empyema are known. Small effusions, in children, produced by pneu- 
mococci may possibly yield to this mild measure, but it is not reliable. 

Recently empyema has been successfully treated by repeated aspira- 
tion followed by the injection into the pleural cavity of several ounces of 
two per cent, formalin in glycerin. The value of the procedure has not 
yet been decided. 

SPECIAL FORMS OF PLEURISY 

Diaphragmatic . Pleurisy. — Pleurisy may affect or be limited to the 
portion covering the diaphragm. The effusion may be of any character, 
fibrinous, serous, or purulent. Two features of the process are important : 
(1) Pain produced by diaphragmatic pleurisy is frequently referred to 
the abdomen and associated with rigidity, especially on the right side, 
has given rise to suspicion of and led to operation for inflammation of the 
appendix or gall-bladder. (2) Physical signs may be lacking or so 
slight as to be overlooked. Thoracic respiration, absence of Litten's 
diaphragm shadow, tenderness over the phrenic nerve in the neck, with 
cough and dyspnea not otherwise explained, are suggestive. (3) The 
symptoms other than the location of the pain are those of any similar 
pleurisy. Obstinate hiccough has, in some cases, resulted from the 
diaphragmatic pleurisy. 

Sacculated Empyema. — Serous pleural exudates are rarely encap- 
sulated, while empyemata are frequently so. The purulent exudate may 
be localized at any part of the chest, even the apex. A curious and rare 
form is that in which the pus is found encapsulated in an interlobar 
fissure, the interlobular empyema. Such localization gives rise to unusual 
localization of the physical signs. The diagnosis must be based on the 
constitutional symptoms taken with the localization of the signs, the 
results of an X-ray examination and finally the exploratory puncture. 
To be successful puncture must be made very deeply, and as the procedure 
must always be attended with some danger, exploratory incision is some- 
times preferable. 

Hemorrhaghic Effusions and Hemothorax.^ — Slight admixture of 
blood with pleural fluids is commonly the result of trauma by the needle. 
Blood may, however, be present in both exudates and transudates of the 
pleura. 

Hemorrhagic pleurisy results (1) from tuberculosis, (2) from cancer. 



DISEASES OF THE PLEURA 



53 



(3) in rare instances from unknown cause. Occasionally after pneu- 
monia or in purpuric conditions, or in pleurisy complicating nephritis, 
cirrhosis of the liver, or heart disease, the fluid may be bloody, but it 
rarely continues so, unless tuberculosis or cancer underlies the process. 
Hemorrhagic transudates are met with at times in cases of nephritis and 
heart disease, or possibly from obstruction of thoracic veins. 

Hemothorax results from the rupture of aneurisms or the erosion of 
intrathoracic vessels, or trauma of the lung or chest wall. Fracture of 
the ribs is especially likely to cause hemothorax by puncture of the lung. 

The symptoms are usually increasing dyspnea and evidences of hemor- 
rhage. The physical signs are those of hydrothorax. The exploring 
needle withdraws blood. After days or weeks the blood may become in- 
fected and empyema result. 

Treatment. — This is usually limited to the aseptic treatment of ex- 
ternal wounds and the management of the general condition. The blood 
in the pleura is left, unless severe dyspnea is caused. It may then be 
aspirated, the blood being drawn off very slowly. The development of 
suppuration will necessitate drainage. 

CHRONIC PLEURISY 

Any form of pleurisy may become chronic. 

Chronic Dry Pleurisy. — After any acute inflammation the pleura is 
left thickened and probably more or less adherent. In some instances the 
affected pleura becomes the seat of chronic inflammation with exacerba- 
tions of acute pleurisy from time to time, resulting in great thickening 
and general adhesions. The process is regularly complicated by intersti- 
tial pneumonia, chronic bronchitis, and possibly bronchiectasis. Apart 
from an occasional stitch in the side the symptoms are limited to those of 
the associated conditions. The physical signs include retraction of the 
affected part of the lung with depression of the chest, limited expansion^ 
dulness on percussion, and diminished voice and breathing sounds. (See 
Interstitial Pneumonia.) At the base such signs indicate, as a rule, a 
simple process; at an apex they regularly signify tuberculosis. In the 
postmortem room more or less general thickening of the pleura with 
adhesions, not recognized during life, is frequently found. 

Chronic Pleurisy with Effusion. — Cases of serous pleurisy or em- 
pyema may be so protracted as to be termed chronic. In such cases the 
pleura becomes greatly thickened, and the lung is compressed and ren- 
dered useless. The patients give the usual symptoms and signs of pleurisy 
and become emaciated and feeble as the result of long illness. 

Treatment. — The general health of the patient nuist be the chief 
object of attention. In the dry form gymnastic and breathing exercises 
are employed to expand the affected part of the lung and prevent re- 
traction. In the serous form, after repented tapping, di-ainnge as for 
empyema may be required. In emy)yema l^^stlander's operation to secure 
the obliteration of the pleural cavity may be called for. 



54 DISEASES OF THE RESPIRATORY TRACT 



HYDROTHORAX 

Definition. — An accumulation of serous fluid not of inflammatory 
origin in the pleura — a transudation. 

Etiology. — The condition is secondary to (1) cardiac or renal disease, 
(2) anemia or other hydremic condition of the blood, or (3) the pressure 
of tumors or new growths upon some of the thoracic veins. The symptoms 
are those of the underlying condition with a gradually increasing dys- 
pnea, due to the accumulating fluid. There is no pain or fever. The 
signs are those of pleurisy with effusion, except that the heart is less 
likely to be displaced. In cardiac hydrothorax the effusion is most often 
on the right side. The pleural fluid is clear serum, alkaline to litmus, 
with a speciflc gravity of 1.010 to 1.015, much albumin, and as a rule an 
excess of endothelial cells. 

Treatment. — The underlying condition must be treated. With severe 
dyspnea the fluid may be aspirated, but will quickly reaccumulate, unless 
the primary affection is controlled. 

PNEUMOTHORAX, HYDROPNEUMOTHORAX, AND 
PYOPNEUMOTHORAX 

Pure pneumothorax is a very rare condition, but collections of serum 
or pus with air or gas in the pleura are not unusual. 

Etiology. — Air or gas may be admitted to the pleura from three 
sources. (1) Through wounds of chest wall or lesions of the lung air 
may enter the pleura. (2) By rupture gas in the stomach or intestine 
may enter the pleura. (3) Finally, infection of pleural exudates by cer- 
tain bacteria, especially the bacillus aerogenes capsulatus, may result in 
the production of gas. The great majority of cases belong in the first 
category, (a) Wounds of the chest wall or lung may admit air at any 
time. Punctures made by the exploring or aspirating needle may do so, 
although these in.struments are more likely to wound the lung, (b) A 
normal lung may rupture under unusual strain, (c) A diseased lung is 
much more liable to such an accident. From 70 to 90 per cent, of all 
cases of pneumothorax are due to the rupture of a tuberculous focus in 
the lung. Bronchopneumonic foci may also yield under strain, espe- 
cially in children suffering from whooping-cough. The tAvo other origins 
of pneumothorax are very rarely seen. When the chest wall or lung is 
penetrated air enters the pleura by reason of the elasticity of the lung 
which leads it to retract and creates a condition of negative pressure in 
the pleura which is met by the entrance of air, until an equilibrium is 
established. By reason of the same tendency on the part of the other 
lung the entrance of air may continue till the affected pleura is somewhat 
distended, the heart crowded to the opposite side and the diaphragm 
depressed. In consequence of a valve-like action of the opening in the 
lung this distention of the affected side may go on to extreme displacement 
of the heart and other adjacent viscera. 



DISEASES OF THE PLEURA 



55 



Morbid Anatomy. — The lung on the affected side is completely re- 
tracted and lies as a shrunken mass in the upper and posterior part of 
the chest. The pleura may be empty, but regularly contains either serum 
or pus. The pleura itself is congested and often coated thickly with 
fibrin, especially in the purulent cases. In the great majority of cases 
the lung presents tuberculous lesions. It may be difficult to locate the 
rupture. The heart is usually displaced to the other side, the diaphragm, 
liver, and spleen depressed. 

Symptoms. — These depend greatly upon the amount of air dra^\Ti 
into the pleura and the resulting displacement of the heart and other 
organs. The onset is usually sudden. Sharp pain in the chest may be 
felt at the time. Dyspnea succeeds, at times so slight that the patient 
continues his occupation, at other times severe. In the milder cases there 
are no other symptoms, in the severe the dyspnea is intense, the face and 
body become livid, pulse rapid and feeble, the extremities cold, the body 
bathed in cold sweat, and the patient is in danger of immediate death. 

Course and Prognosis. — If the patient survives the initial shock, the 
outcome depends upon the nature of the lesion. In the spontaneous cases, 
or in those produced by wounds of an aspirating needle, the air is usually 
absorbed and the patients are soon well. Pneumothorax resulting from 
accidental puncture of the lung in aspiration may prove a dangerous or 
possibly fatal complication of pleurisy with effusion or hydrothorax. 
The tuberculous cases, the great majority, do badly. The pleura becomes 
infected, the patients suffer from pyopneumothorax as well as tuber- 
culosis, and gradually failing die \^dthin a few weeks or months. 

Physical Signs. — Inspection. — The affected side may bulge and is 
immobile. The pulsation of the displaced heart may be noted. Cyanosis, 
dyspnea, and profound exhaustion may be present. 

Palpation. — The heart beat is located in an unusual position. (See 
Fig. 14.) Vocal fremitus is absent over the air-containing chest, also over 
the area of fluid, if this be present. The liver or spleen is depressed so 
as to be palpable. 

Percussion. — Over the air-filled chest, the note is tympanitic, hyper- 
resonant, or dull. The area of resonance is larger than normal, if the 
pleura is distended. If fluid be present, there is dulness over it, shifting 
as the position of the patient is changed. The heart dulness is displaced 
or lost. 

Auscultation yields the most characteristic signs of pneumothorax. 
The respiratory murmur is faint and may be lost over the air, but is 
frequently amphoric. It will be lost over fluid. The voice sounds are 
similarly faint and distant, but may be amphoric. Moist rales may be 
heard and the metallic tinkle of Laennec. The coin test gives positive 
results. Thus the clink produced by holding one coin on the chest in 
front and tapping it lightly with another is heard clearly if one listens 
over the posterior chest. On shaking the patient a succussion or splashing 
sound is heard if fluid is present with the air. The metallic tinkle, the 
coin test and succussion are practically pathognomomc of hydropneu- 
mothorax. 



56 



DISEASES OF THE RESPIRATORY TRACT 



Diagnosis. — With characteristic physical signs the diagnosis of 
pneumothorax is easy. Pleurisy with effusion may give similar signs, but 
without the metallic tinkle, coin test, or succussion. Dilated stomach may 
sometimes give such signs in the lower left chest, but the tympany is 
continuous with that of the stomach in the abdomen with the usual evi- 
dences of dilatation of the stomach. Diaphragmatic hernia admitting 
the stomach and intestines to the thorax may easily be mistaken for 
hydropneumothorax. Variations in the signs, the presence of borbo- 
rygmi and the results of fluoroscopy after a bismuth meal will identify 
the condition. Subphrenic abscess containing gas may present a very 
difficult problem. Here a previous history of gastric or intestinal ulcera- 




FiG. 14. — Pyopneumothorax: left pleura filled by pus (and air) concealing the lung; the heart 
pushed far to right and covering all but the anterior edge of the lung; the left side of diaphragm, left 
lobe of liver, stomach, spleen and colon pushed downward and to right. From the collection of Dr. 
Walter B. James. 

tion, absence of pulmonary symptoms, the normal situation of the hearty 
and epigastric pain and tenderness should lead to a correct diagnosis. 

Treatment. — Rest in bed and good care suffice for the simpler cases. 
If much fluid be present, or if the displacement due to air be extreme,, 
aspiration is indicated and may be repeated as often as necessary. Opera- 
tive treatment, other than aspiration, is rarely helpful, since the wound in 
the lung fails to close, the pleura, if not already infected, becomes so and 
the patient dies of protracted suppuration. For the great majority the 
after-treatment is that of pulmonary tuberculosis. 



PLATE I. 




A, Parasitic stomatitis. 



Lesions of the Mouth. 
B, Ulcerative stomatitis. 
D, Geographical tongue. 



C, Aphthous stomatitis. 



II 

DISEASES OF THE DIGESTIVE SYSTEM 



DISEASES OF THE MOUTH 

STOMATITIS 

Inflammation of the mucous membrane of the mouth occurs in 
various forms and under many different conditions. It is seen in such 
general diseases as scarlet fever, diphtheria, scurvy, etc. ; in various 
digestive disturbances; as a result of local irritation or infection of 
various sorts, and after the administration of such drugs as mercury. 

Catarrhal Stomatitis. — Simple inflammation of the buccal mucosa 
is seen at all ages and is caused by various local irritants, by dentition, 
by digestive disturbances, etc. It is often seen in the infectious diseases. 
Usually a large portion of the mucosa of the mouth and tongue is 
involved and is bright red, and swollen, tender and painful. Con- 
stitutional symptoms are slight or lacking. Treatment consists in the 
careful cleansing of the mouth after feeding and in the frequent use 
of a simple mouth wash such as lime water, or a solution of sodium 
bicarbonate or borax (gr. x-gi). 

Herpetic Stomatitis (Aphthous Stomatitis). — This is a condition 
common in young children and marked by the appearance of small 
herpetic vesicles upon the edges of the tongue and inner surface of 
the lips and cheeks. Within a day or two the vesicles break and 
superficial ulcers with a grayish base and red periphery are formed. 
There are usually several crops of such vesicles and the condition lasts 
a week or two. (See Plate I.) There is pain and burning in the mouth, 
increased salivation and difficulty in taking food. There may be slight 
fever. The mouth should be frequently cleansed with some simple mouth 
wash and the vesicles or ulcers touched ^xith nitrate of silver or powdered 
burnt alum. 

Ulcerative Stomatitis. — This is a more severe form of inflammation 
which may occur at any age, but which is chiefly seen in children. 
Most of the cases are met with among children of the lower classes, 
and malnutrition from, any cause, and a lack of cleanliness of the teeth 
and mouth are the chief predisposing factors. The same condition 
is seen in scurvy and in mercurial poisoning. The gums become swollen 
and spongy and there appear at the edges of the gums and between the 
teeth small, irregular ulcers having a dirty gray base and ragged edges. 
In severe cases the ulcers may extend to the inner surface of the cheeks 
and to the tongue; the teeth may loosen and there may even be necrosis 
of the alveolar process. (See Plate I.) 

57 



58 



DISEASES OF THE DIGESTIVE SYSTEM 



Profuse salivation and fetid breath are the most noticeable symptoms. 
The gums bleed readily ; there is great pain and discomfort in taking 
food; the submaxillary lymph-glands are swollen, and there is usually 
some fever. The disease, unless properly treated, may last many weeks 
and may even threaten life. 

Treatment. — Everything possible should be done to improve the 
general health and to remove the primary cause. The mouth should be 
frequently washed with peroxide of hydrogen, diluted two to five times, 
or a weak solution of potassium chlorate or of alum. Internally 
potassium chlorate acts as a specific and should be given in small and 
frequently repeated doses (gr. ii-v). Under such treatment recovery 
is usually prompt and complete. 

Parasitic Stomatitis (Thrush). — Thrush occurs chiefly in infants 
during the first few months of life. It is due to infection by a fungus, 
saccharomyces albicans, which gains entrance to the mouth by means of 
nursing bottles, soiled nipples, etc., or through the air. Some slight 
inflammation of the mucosa or lack of cleanliness seems necessary for 
infection. The fungus is composed of branching threads (mycelium) 
and spores. It invades the epithelial layer of the mucosa and forms 
small patches of milk-white color which unite to form large areas. The 
process is seen chiefly upon the dorsum of the tongue, sides of the cheeks 
and hard palate, but may extend to the wall of the pharynx and even 
down the esophagus to the stomach. This white pellicle, which looks 
like coagulated milk, is quite firmly attached to the mucous membrane 
and when removed is apt to leave bleeding points. ( See Plate I. ) The only 
symptoms are those of some discomfort in taking food. The condition 
is of much importance in poorly nourished and sickly infants in whom 
the disinclination to nurse may be a serious matter. 

Treatment. — The disease is much more easily prevented than 
cured. If nursing bottles, rubber nipples, etc., are properly disinfected, 
and the mouth cleansed after each feeding, thrush is not likely to 
develop. When it exists a saturated solution of boric acid or some 
other mild antiseptic should be applied several times a day and the 
mouth should be cleansed after each feeding with a solution of borax 
or of sodium bicarbonate (gr. x-gi). 

Gangrenous Stomatitis (Cancrum Oris, Noma). — This is a rare and 
fatal affection occurring in children and characterized by a rapidly 
spreading gangrene of the mouth and cheeks. The disease develops in 
children whose vitality and resisting powers have been much lowered 
by some illness, and is usually seen after some such infectious disease 
as measles. The Streptococcus pyogenes or an organism resembling 
closely the diphtheria bacillus is usually found. The process begins in 
the mucous membrane of the cheek or gums as a small spot of gangrene 
Avhich extends rapidly until a large portion of one or both cheeks is 
destroyed. The surrounding tissues are edematous and inflamed. The 
process usually shows no tendency to self-limitation, but occasionally the 
slough may separate and the remaining ulcer cicatrize and heal. The 



DISEASES OF THE SALIVARY GLANDS 



59 



symptoms are those of profound sepsis. There are high fever, extreme 
prostration and a sickening fetor to the breath. Most of the cases die 
within a week or ten days. 

Treatment is altogether unavailing unless the disease is recognized and 
radically treated by excision and cauterization in its earliest stage. The 
patient's strength should be supported by careful feeding and free 
stimulation. 

Acute Glossitis. — An acute inflammation of the tongue is occasionally 
seen as the result of trauma, of the taking of too hot food or drink or 
of some corrosive substance. It also occurs in mercurial stomatitis. 
The tongue is much swollen, red, and indented by the teeth. Salivation 
is increased and there are great pain in taking food and difficulty in 
swallowing. The condition usually subsides within a few days and no 
treatment is needed except a simple astringent mouth wash. 

Geographical Tongue. — This is a sub-acute or chronic affection of 
unknown origin, seen occasionally both in children and in adults. Upon 
the dorsum of the tongue there appear bright red areas of circular 
or crescentic outline with gray borders, which gradually spread, coalesce 
and change their outline. The red areas are due to desquamation of 
the superficial epithelium, the gray borders to thickening of the 
epithelium_. (See Plate I.) Aside from some slight sensitiveness of the 
tongue there are no symptoms. The condition subsides within a few 
weeks or months. 

Leukoplakia Buccalis. — This chronic affection of the tongue is seen 
most frequently in heavy smokers. A similar condition is met with in 
sjrphilis. Slightly elevated, irregular whitish patches appear upon the 
dorsum, due to thickening of the superficial epithelium, which run a 
very chronic course, cause more or less discomfort in eating and are very 
resistant to treatment. Rarely the condition has terminated in 
epithelioma. 

DISEASES OF THE SALIVARY GLANDS 

Disturbances of the Salivary Secretion. — Excessive secretion of 
saliva {Salivation, Ftyalism) may result from the use of such drugs as 
mercury, pilocarpine, tobacco and potassium iodide ; is often seen in 
pregnancy and insanity, and occurs in inflammations of the mouth and 
in hydrophobia. 

A lack of salivary secretion (xerostomia) is seen in fevers, in certain 
stomach disorders, in diabetes and in poisoning by belladonna and 
stramonium. 

Inflammation of the Salivary Glands. — The parotid is the gland 
chiefly affected. 

Acute Parotitis. — Aside from the specific form (mumps) parotitis 
occurs as a secondary affection in typhoid fever, pneumonia and many 
other infectious fevers, and occasionally in injuries and diseases of the 
genital organs and abdominal viscera. Infection may occur from the 
mouth along Stenson 's duct, or by means of the blood. In many of these 



60 



DISEASES OF THE DIGESTIVE SYSTEM 



ca.ses the iflammation goes on to suppuration and pus may be expressed 
from the duet. Usually the process subsides within a week or ten days. 

Chronic Px\rotitis may result from the acute form or from poisoning 
by mercury or lead. 

Von IMikulicz's Disease is a rare and curious affection characterized 
by the slow and symmetrical enlargemeut of all the salivary, and of the 
lachrymal, glands. Its cause is unknown. The parotid gland may be the 
seat of both benign and malignant tumors. 

DISEASES OF THE PHARYNX 

PHARYNGITIS 

Acute Catarrhal Pharyngitis. — This may result from exposure alone, 
but is favored by such conditions as gout, rheumatism and digestive dis- 
turbances. The inflammation may be confined to the pharynx or may 
involve also the tonsils, soft palate. Eustachian tubes, larynx, etc. Con- 
stitutional disturbance is usually slight, but there are pain, dryness and 
tickling in the throat, discomfort in swallowing and often soreness of 
the muscles of the neck. The trouble usually subsides within three or 
four days. 

A- brisk purge at the outset, salol or aconite in small doses and a 
simple throat spray are all that is needed in the way of treatment. 

Chronic Pharyngitis. — Chronic inflammation of the pharynx is fre- 
quently seen in heavy smokers, in clergymen, public speakers and others 
who use the voice excessively and in those of a gouty or lithemie diathesis. 
The mucous membrane is congested and covered with thick, tenacious 
mucus. In some eases it is much thickened ; in others, it is thin, dry and 
shiny (pharyngitis sicca), and in others many minute, projecting red 
areas are seen {granular pharyngitis) . The small projections are com- 
posed of masses of lymphoid cells. The symptoms are those of dryness 
and tickling in the throat with the constant inclination to cough and 
clear the throat. Sometimes the constant accumulation of mucus causes 
much discomfort. Hoarseness and cough are often the result of an asso- 
ciated laryngitis. In the treatment attention must be paid to the removal 
of the cause and the improvement of the general health. Occasional 
applications of a solution of nitrate of silver (10 per cent.) should be 
made to the pharynx and the throat should be kept free of mucus by the 
frequent use of a simple spray. 

Retro-pharyngeal Abscess. — Two distinct varieties occur: (1) an 
acute form seen in infants and (2) a chronic form secondary to caries of 
the cervical vertebrae. 

TiiK ACUTE FORM IS sccu in children of less than three years and begins 
as an infection of the retro-pharyngeal lymph- glands, which does not 
always go on to suppuration. The general symptoms are those of fever 
and prostration and the local symptoms those of nasal and laryngeal 
ol)stru('ti(m aud difficulty in swallowing. There are nasal \^oice, mouth 



DISEASES OF THE TONSILS 



61 



breathing, dyspnea which is chiefly inspiratory, and difficult and painful 
deglutition. Inspection of the pharynx and examination with the finger 
reveal a fluctuating tumor mass projecting forward from the posterior 
pharyngeal wall. The swelling may show externally below the angle of 
the jaw and there may be stiffness of the neck. The diagnosis offers no 
difficulties if the possibility of the condition is borne in mind, and the 
throat examined by the eye and finger. 

Treatment consists in the prompt evacuation of the abscess by incision 
through the mouth. 

The chronic form is much rarer, occurs at any age, is usually much 
larger and is associated with little or no fever. The spine gives evidences 
of caries. 

DISEASES OF THE TONSILS 

ACUTE FOLLICULAR TONSILLITIS 

Etiology. — This is an extremely common affection seen chiefly in older 
children and young adults. Exposure to cold and damp, unhygienic sur- 
roundings, tonsillar hypertrophy and rheumatism seem to be predisposing 
causes. Individual predisposition varies greatly. The disease often 
attacks several members of a household. 

Morbid Anatomy. — The inflammation involves the crypts and sur- 
face of the tonsils, which are red and somewhat swollen. At the mouth 
of the crypts small yellowish-white plugs appear, which consist of epi- 
thelial and pus cells, mucus and fibrin. Both tonsils are affected. 

Symptoms. — The onset is abrupt with chilliness, headache, pains in 
the back and limbs and a rapid rise of temperature to 102°-104°. The 
tongue is coated and there are anorexia and constipation. The general 
symptoms are usually quite out of proportion to the local ones, which 
consist only of soreness of the throat and discomfort in swallowing. The 
surface of the tonsil is studded with yellowish- white points, some of which 
may fuse together, but there is no true pseudo-membrane and the points 
can be readily wiped away with a swab. Most of the symptoms subside 
in three or four days and the whole duration of the disease is less than a 
week. Otitis media is an occasional, and endocarditis a rare complication. 
The differential diagnosis from diphtheria is given under that heading. 

Treatment. — Rest in bed, a fluid or semi-fluid diet and an active purge 
at the outset are the chief requisites. Small doses of aspirin 
or sodium salicylate are given at frequent intervals. The pains may be 
relieved by phenacetin. The throat should he sprayed with some simple 
alkaline solution or with dihite hydrog(Mi ])er()xide. A cold compress may 
be applied to the neck, or hot applications such as a poultice 
of flaxseed or kaolin (see Appendix) may give comfort. 



62 



DISEASES OF THE DIGESTIVE SYSTEM 



SUPPURATIVE TONSILLITIS 
(Quinsy) 

The etiology is similar to that of follicular tonsillitis. 

The inflammation begins deep in the substance of the tonsil or in the 
peritonsillar tissue and in most cases goes on to the formation of an 
abscess. Usualh^ only one tonsil is attacked. 

Symptoms. — The onset does not differ from that of follicular ton- 
sillitis. Soon, however, the local symptoms become much more pro- 
nounced. There is constant severe pain in the throat, great difficulty in 
swallowing, stiffness and tenderness of the neck and difficulty in opening 
the mouth. One tonsil and the surrounding tissues then become greatly 
SAVollen and may extend to or beyond the median line, the uvula being 
displaced to the opposite side. At first the swelling is firm and braA^TLy, 
but after several days an area of softening can usually be recognized on 
the anterior surface. The abscess if left to itself breaks in from five to 
seven days, and this is usually followed by prompt relief of all the symp- 
toms, both general and local, and by rapid convalescence. The patients 
regularly recover. Rarely death has occurred from edema of the glottis 
or from perforation of the carotid artery. Occasionally the process is 
repeated in the other tonsil. 

Treatment. — In addition to that given for follicular tonsillitis, the 
pain and distress may be somewhat mitigated by hot fomentations or an 
ice-bag to the neck, and by codeine or Dover's powder at night. As soon 
as any point of softening can be felt by the finger the tonsil should be 
freely incised and the pus evacuated. 

HYPERTROPHY OF THE TONSILS AND ADENOID 
^^:GETATIONS 

Chronic enlargement of the tonsils and adenoid growths of the naso- 
pharynx are usually found associated and produce similar symptoms. 

Etiology. — These conditions occur chiefly in children up to the time 
of puberty. A marked predisposition to lymphoid hyperplasia is seen 
in certain families and individuals. Damp dwellings, bad air and fre- 
quent acute inflammations of the nose and throat are the predisposing 
causes. 

Morbid Anatomy. — The adenoid growths are similar in structure 
to the tonsils and in both there is hyperplasia of the lymphoid tissue and 
the connective-tissue stroma in varying proportions. The tonsils are 
much enlarged and the adenoid growths may almost completely fill the 
naso-pharynx. 

Symptoms. — There is a tendency to frequent attacks of tonsillitis 
and of nasal and pharyngeal catarrh. Obstruction of the posterior nares 
by the adenoid growths results in mouth-breathing, snoring, restless 
sleep, night terrors, a hoarse, nasal voice, deafness, a dull, apathetic 
facial expression, a high, narrow palatine arch and certain deformities 



DISEASES OF THE ESOPHAGUS 



63 



of the chest (pigeon breast). The breath is often very offensive and 
there may be various reflex symptoms. Acute otitis media is a frequent 
sequel. The diagnosis of adenoid growths is verified by digital examina- 
tion of the naso-pharynx. 

Treatment. — The milder grades of tonsillar and adenoid enlarge- 
ment may be somewhat relieved by general tonic treatment, by the use 
of the syrup of the iodide of iron (gtt. x-xx t. i. d.) and especially by 
removal to a warm, dry climate during the winter months. When the 
symptoms are pronounced, however, the operative removal of both the 
adenoids and the tonsils is demanded, since very serious and permanent 
damage to the child may thus be prevented. 

DISEASES OF THE ESOPHAGUS 

ACUTE ESOPHAGITIS 

This is most frequently seen as the result of the swallowing of cor- 
rosive poison or of very hot fluids. It is seen occasionally in the course 
of such diseases as typhoid fever, pneumonia and small-pox. A phleg- 
monous type sometimes complicates ulcer or cancer of the esophagus. 
The inflanunation may be of a catarrhal, suppurative or pseudo-mem- 
branous type. 

The chief symptom is a constant, dull or burning pain behind the 
sternum which is much increased by every effort to swallow food. There 
is usually more or less fever. If ulceration develop the resulting 
cicatrization usually leads to stricture. 

ULCERATION OF THE ESOPHAGUS 

Ulceration is rare except as a result of corrosive poisons or of cancer. 
It may occur, however, in typhoid fever, small-pox, diphtheria, syphilis, 
and tuberculosis. An ulcer similar in nature to the peptic ulcer of the 
stomach is sometimes seen at the lower end. 

Varicosities of the esophageal veins often occur in cirrhosis of the 
liver with portal obstruction, and profuse and even fatal hemorrhage 
may result from their rupture. 

SPASM OF THE ESOPHAGUS 

Aside from hydrophobia this rare condition is met with chiefly in 
hysterical or hypochondriacal patients of either sex. There is a sudden 
contraction of the muscular coat which prevents the swallowing of solid 
food or even of liquids. It is paroxysmal in its appearance; occurs 
especially when the patient is excited or nervous, and is often associated 
with thoracic pain. The nutrition usually does not suffer. The condi- 
tion is recognized by the history and by the fact that the spasm will 
yield to the steady, gentle pressure of an esophageal bougie. The treat- 
ment is that of the underlying nervous state. 



64 



DISEASES OF THE DIGESTIVE SYSTEM 



STENOSIS OF THE ESOPHAGUS 

In addition to the spasmodic stricture just described, obstruction of 
the esophagus may result from (a) cicatricial contraction; (b) cancer 
or other new growth in the wall; (c) pressure from without, by thoracic 
aneurism, mediastinal tumor, pericarditis with effusion, goitre, etc., and 
(d) foreign bodies. 




Fig. 15. — Stricture and dilatation of the esophagus, demonstrated by the X-ray after the inges- 
tion of an emulsion of bismuth subcarbonate, which being imper\'ious to its rays appears as a dark 
shadow. The patient lies obliquely upon the right side and the X-ray tube is close to the left shoulder, 
which is therefore most distinct. The curvature of the spine results from the position. 

Cicatricial Stricture. — The extensive ulceration which follows the 
swallowing of some corrosive poison is the usual cause. The stricture is 
commonly near one or the other end of the esophagus, and the tube 
above is apt to be dilated and its muscular wall hj^pertrophied. There 
is increasing difficulty in the swallowing of solid food. If there is much 
dilatation above the stricture the food may be retained for some time 
before it is regurgitated. Such regurgitated material will be undigested 
and free from hydrochloric acid and from the characteristic odor of 
stomach contents. The position and calibre of the stricture may be 
recognized by the careful passage of graduated esophageal bougies. The 
treatment is surgical. 



DISEASES OF THE STOMACH 



65 



Cancer of the Esophagus. — This occurs usually in advanced life 
and is commoner in men. The growth begins in the mucous membrane, 
is of the type of epithelioma and is commonly seen in the lower third 
of the tube. From its annular form it tends to early and progressive 
stricture, which, however, is sometimes temporarily relieved by the 
ulceration to which the tumor is prone. This ulceration may perforate 
the wall and cause infection of the cellular tissue of the neck, the pos- 
terior mediastinum, the pericardium, lung or trachea, etc. 

The SYMPTOMS are those of increasing difficulty in swallowing solid, 
and later liquid, food, together with progressive emaciation and more 
or less pain. The regurgitated food may be mixed with blood or pus, 
and the tip of the exploring sound may be blood stained. Death results 
from starvation or from some of the complications due to perforation. 

The DIAGNOSIS is made by excluding the other above-mentioned causes 
of obstruction and by considering the age of the patient. The possibility 
of the presence of a foreign body or an aneurism should be remembered. 
The disease is always fatal. 

Treatment is purely palliative. So long as liquid food is swallowed 
without difficulty nutrition may be fairly well preserved. Sometimes 
feeding may be accomplished by means of a small stomach tube passed 
beyond the point of stricture. When swallowing becomes inadequate 
gastrostomy should be performed, since rectal feeding cannot be main- 
tained for any length of time. The pain may require morphine. 

Diverticulum. — This rare condition is usually due to pressure, ex- 
erted during swallowing, and occurs in the posterior wall at the junction 
of pharynx and esophagus, Avhere the muscular coat is deficient. It may 
reach large size. Small diverticula are sometimes seen on the anterior 
w^all due to traction exerted by inflamed and adherent bronchial glands. 

Dilatation of the esophagus is seen often above a stricture, but 
occurs rarely also as a primary condition ^vithout known cause. Stric- 
ture and dilatation of the esophagus can be beautifully shown by a 
radiograph immediately following the ingestion of a paste or gruel con- 
taining an ounce of bismuth subcarbonate. (See Fig. 15.) 

DISEASES OF THE STOMACf^ 

ACUTE GASTRITIS 
(Acute Indigestion. Acute Gastric Catarrh ) 

Etiology. — Acute gastritis is common at all ages, but is especially 
frequent in children. Its prevalence is greatest during the hot months. 
Gout, tuberculosis, and other chronic diseases, and such conditions as 
produce passive c(mgestion of the stomach (valvular disease, cirrhosis 
of the liver, etc.) are all predisposing causes. Individual predisposition 
is frequently seen. The condition not infrequently occurs in the course 
of the infectious fevers. Some error in diet is the usual exciting cause. 
This may be food, excessive in quantity or irritating in character, such 
as unripe or over-ripe fruit, sour milk, tainted meat, etc. Alcoholic 
5 



66 



DISEASES OF THE DIGESTIVE SYSTEM 



excess is a common cause. In certain persons special articles of diet, 
such as shell fish, etc., will always excite an acute gastric catarrh. 

Morbid Anatomy. — The process is similar to that of an acute catar- 
rhal infiammation of any other mucous membrane. The mucosa is 
swollen, hyperemic and infiltrated with serum and leukoc;>i:es. The sur- 
face, at first dry, is later covered with thick, glairy mucus. The cells 
of the mucous and peptic glands undergo cloudy swelling and the secre- 
tion of hydrochloric acid and pepsin is diminished or entirely abolished. 

Symptoms. — Anorexia, nausea and vomiting are the chief symptoms. 
The first two are almost never absent. In severe cases vomiting is con- 
stant and persistent and there are moderate fever, much prostration and 
more or less epigastric pain and tenderness. In the mild cases vomiting 
ma}^ occur only at the outset or may be absent altogether, and there is 
usually 'little or no fever. The tongue is heavily coated ; the breath foul ; 
thirst is often distressing, and the bowels may be either constipated o*r 
loose. The vomited matter consists at first of undigested food and later 
of mucus (which may be blood-streaked) and bile. There is often an 
absence of free hydrochloric acid. The symptoms usually last only two 
or thi^e days, but occasionally they may persist for a week or two, or 
even longer. Complete recovery is the rule, but repeated attacks may 
lead to a chronic gastritis. 

Treatment. — At the outset, if vomiting has not occurred, the stomach 
should be emptied by the use of a simple emetic, and the bowels should 
be freely moved by calomel, blue mass or a saline. Complete rest to the 
stomach is the most essential part of the further treatment. Often it is 
best to withhold all food for 2i hours and then to begin with milk or 
broths in minute and frequently repeated doses. If the onset is violent 
a small dose of morphine subcutaneously will often check the vomiting. 
In other cases rectal feeding may be needed for two or three days. 
Vomiting may sometimes be checked by a mustard paste applied to the 
epigastrium or by dilute hydrocyanic acid (lUj-ij), bismuth subnitrate 
(gr. x-xx) or cerium oxalate (gr. v). The return to solid food should 
be made gradually and cautiously and its digestion is often aided by 
the use of dilute hydrochloric acid. 

Special Types. — Toxic Gastritis. — A very intense form of inflam- 
mation is that due to the ingestion of the violent irritant poisons, such 
as the mineral acids, the caustic alkalies, carbolic acid, phosphorus, 
arsenic, corrosive sublimate, etc. There are necrosis and destruction of 
portions of the mucosa, inflammatory swelling of the surrounding areas, 
and submucous hemorrhages. There are also often excoriations of the 
lips, tongue, pharynx and esophagus. 

The SYMPTOMS consist of intense pain in the throat and epigastrium, 
persistent retching and vomiting, difficulty in swallowing and j^rostra- 
tion amounting often to collapse. The vomitus is often streaked with 
blood and may contain shreds of necrotic tissue or evidences of the 
poison. If the ease is not immediately fatal, ulceration, chronic gastritis 
or esophageal stricture may result. 



DISEASES OF THE STOMACH 



67 



The TREATMENT consists in the prompt washing of the stomach, the 
use of the appropriate antidotes, the relief of pain by morphine, and 
rectal feeding. 

Phlegmonous Gastritis is an extremely rare affection in which 
suppuration, either circumscribed or diffuse, occurs in the submucous 
tissue. The cause is usually obscure. The vomitus may contain pus, 
but the condition is rarely recognized during life. 

Croupous or Membranous Gastritis occurs rarely in diphtheria and 
in such conditions as pneumonia and small-pox. 

Parasitic or jMycotic Gastritis may be seen as the result of the 
growth of certain fungi. 

CHRONIC GASTRITIS 
(Chronic Gastric Catarrh. Chronic Dyspepsia) 

Etiology. — Chronic catarrhal inflammation of the stomach may be 
primary or may be secondary to one or more attacks of acute gastritis 
or to gastric ulcer or cancer. The primary cases are due regularly to 
long-continued dietetic errors. Of these the abuse of alcohol is perhaps 
the most frequent; out habitual overeating, hurried eating, insufficient 
mastication, the excessive use of fried dishes, of pastries, of hot breads, 
of tea and coffee and of ice-water are common and important causes. 

Among the predisposing causes are to be mentioned such constitu- 
tional disturbances as gout, diabetes, chronic nephritis, chronic tuber- 
culosis and anemia, and such conditions as produce passive congestion 
of the stomach (cirrhosis of the liver and chronic heart affections). 

Morbid Anatomy. — The changes are usually most distinct in the 
pyloric portion. The mucous membrane is of grayish color, is coated 
with thick, tough mucus, and may shoAv areas of congestion or pigmenta- 
tion. It is also often thickened and wrinkled and may even present 
polypoid projections. Small, superficial erosions are sometimes seen. 
Microscopically the glands show various degrees of degeneration and 
atrophy and there are a round-celled infiltration and connective-tissue 
proliferation in the interstitial tissue between and beneath the glands 
and in the submucous and even the muscular layer. In certain cases this 
connective-tissue proliferation leads to great sclerosis and thickening of 
the stomach wall. This thickening may be confined to the pyloric region 
and may result in stenosis with secondary dilatation of the stomach, 
or rarely it may involve the whole stomach and cause great contraction 
of the organ (cirrhosis ventricidi). In other cases the inflammatory 
changes result in great thinning and atrophy of the mucous and mus- 
cular coats with almost complete obliteration of the gastric tubules 
(atrophic gastritis). 

Symptoms. — The disease begins very insidiously and the symptoms 
vary greatly in different cases and are often vague and indefinite. 
Nausea, vomiting, a sense of weight and fullness, dull pain, eructations 



68 



DISP]ASES OF THE DIGESTIVE SYSTEM 



of gas and sour fluid, and flatulence are the most common sjTiiptoms. 
Vomiting may be slight or lacking or may be of daily occurrence. In 
alcoholic cases it often occurs before breakfast. Pain when present is 
referred to the epigastrium and is usually of a dull, burning character. 
It may be the chief symptom and usually appears from one to three 
hours after eating. A moderate degree of epigastric tenderness is com- 
iTion. The tongue is usually coated, there is often a bitter taste in the 
mouth, the breath is offensive and the pharynx is usually congested and 
coated with mucus. The bowels are apt to be constipated, but diarrhea 
may result from the irritation of undigested and fermenting food in the 
intestine. The appetite is usually much disturbed, there is some loss of 
flesh, and headache and mental depression are common. Certain cases 
of atrophic gastritis are associated with a very severe and pernicious 
form of anemia. 

Examination of the Stomach Contents. — The vomited matter is 
neutral or slightly acid in reaction, consists of partly digested food 
mixed with more or less thick, glairy mucus and may contain bile and 
rarely traces of blood. In the stomach washings there is almost always 
more or less mucus. After a test meal the expressed contents show 
usually a marked deficiency of both hydrochloric acid and pepsin ; occa- 
sionally, however, HCl may be normal or increased in amount. In 
atrophic gastritis there may be complete absence of HCl and of pepsin 
and the milk-curdling ferment (acJiylia gastrica). If pyloric obstruc- 
tion or atony of the stomach wall exists the food is delayed in the 
stomach, undergoes fermentation with the formation of abnormal or- 
ganic acids, and the stomach Avashings will contain food remains even 
seven or eight hours after a full meal. 

Course. — Chronic gastritis once thoroughly developed usually persists 
indefinitely. Improvement may be secured by treatment and complete 
recovery is possible, but in most cases the condition improves only tem- 
porarily and frequent relapses occur. The patients become thin, anemic: 
and possibly emaciated, suffer more or less constantly, and as a rule 
become extremely irritable and unhappy. The condition is rarely fatal in 
itself. The patients in the end succumb to intercurrent disease. 

Diagnosis. — The presence of considerable amounts of mucus in the 
stomach washings, the diminution or absence of HCl in test analyses, the 
long duration of the symptoms and the absence of the usual evidences 
of gastric ulcer, cancer or dilatation are the points of special diagnostic 
value. 

Treatment. — General Management. — Careful attention should be 
given to the removal of the cause if that can be discovered. The teeth 
should be put in good condition, the food eaten slowly and mastication 
performed thoroughly. A short rest both before and after eating, and 
a certain amount of regular exercise and recreation should be insisted 
upon. 

Diet. — No hard and fast rules can be laid down. In severe cases it 
may be wise to confine the diet for a time to skimmed milk, milk and 



DISEASES OF THE STOMACH 



69 



vichy, buttermilk or koumyss. In most cases it is only necessary to 
have the meals light, well cooked and easily digestible, and to exclude 
such unsuitable articles as hot breads and cakes, pastries, fried foods, 
fats, pork, veal, etc. Sugar and starches should be used sparingly if 
there is much fermentation and tlatulence. Alcohol, coffee and tea 
should be taken only in very small quantities if at all. 

Lavage. — In most cases lavage is of great value. It is especially 
useful in cases in which mucus is abundant or in which there is a ten- 
dency to the retention of food beyond the normal period. The water 
should be warm and should be made alkaline by sodium bicarbonate 
(Ji to the quart). Weak solutions (1-2000) of nitrate of silver are 
also used. The washing is best done at bedtime or before breakfast. 

Medicines. — Hydrochloric acid is useful whenever its secretion is 
deficient. Twenty or thirty minims of the dilute acid should be given 
after meals. Pepsin is rarely lacking in the gastric juice and is there- 
fore not often required. Sodium bicarbonate and the bitter tonics 
given before meals are often an effective stimulant to gastric secretion. 

Pain may usually be relieved by bismuth subnitrate or by small 
doses of cocaine. Constipation is to be combated by a laxative diet 
(cooked fruits, buttermilk, honey, etc.) and by a simple aloin or cascara 
tablet at night or a mild laxative water before breakfast. Flatulence and 
acid eructations may be controlled by sodium bicarbonate, but the fer- 
mentation giving rise to these symptoms is often best prevented by the 
use of hydrochloric acid, 

ULCER OF THE STOMACH 
(Peptic Ulcer. Round Ulcer ) 

In addition to such ulcers as those of tuberculosis, syphilis and 
typhoid fever, which are all extremely rare in the stomach, there exists 
an important and relatively common form — the peptic ulcer — which is 
peculiar to the stomach and duodenum and whose causation is still 
uncertain and obscure. 

Etiology. — The disease is met with most frequently between the 
ages of twenty and thirty years, although it is not uncommon during 
the next decade and may occur at any age. It was formerly thought 
to be much more frequent in women than in men. Chi orotic girls of 
the servant class seem especially susceptible. It is sometimes met with 
in shoemakers, tailors and others whose occupation leads to continued 
pressure upon the epigastrium. It has been known to follow blows and 
other traumata of the abdomen. Of patients requiring surgical inter- 
vention the great majority are men. 

Pathogenesis. — The origin of the gastric ulcer is still uncertain. It 
is generally believed that the direct cause is the digestion of a portion 
of the mucosa by the gastric juice, but the reason for such self-dig(^stion 
is often not clear. In some, but by no means all, of the cases this is 
due to thrombosis or embolism of the arterial branch supplying the 



70 



DISEASES OF THE DIGESTIVE SYSTEM 



affected region. Changes in the character of the blood, such as chlorosis 
and other forms of anemia, and hyperacidity of the gastric juice are 
regarded as important predisposing causes. Local infection by bacteria 
has been suggested as a possible cause. 

Morbid Anatomy. — The ulcers are usually single, but two or more 
are not infrequently seen. They occur usually in the pyloric region and 
most frequently on the posterior wall near the lesser curvature. In the 
great majority of cases subjected to operation for ulcer the lesion is 
found not in the stomach but in the duodenum (80 per cent, of the 
cases operated upon by the Mayo brothers). Two forms, the acute and 
the chronic, are recognized. The acute ulcer is usually small (from 
one-third to one inch in diameter) and round, and has clean-cut, 
" punched-out " edges and a smooth base. The chronic ulcer is often 
larger, the outlines are irregular, the edges much thickened and in- 
durated and the floor uneven and often terraced. The floor may be 
formed by the submucous, muscular or peritoneal coat or by the surface 
of some adherent organ such as the pancreas or liver. If the ulcer heals, 
a scar of varying extent and thickness is left which may result in ob- 
struction of the pylorus or, rarely, in hour-glass constriction of the 
stomach. Instead of healing, however, it may perforate the stomach 
wall. Such perforation, especially if on the anterior surface, may result 
in general peritonitis, or it may cause a localized abscess, fistulous com- 
munication with the colon or duodenum or rarely perforation of the 
pleura or pericardium. 

Symptoms. — Dyspeptic symptoms, vomiting, pain and hematemesis 
constitute the usual symptoms. 

Pain. — This is the most constant symptom and is rarely altogether 
absent, although it varies much in character and severity in the different 
cases. In its most characteristic form it is a severe, boring pain coming 
on a short time (from 15 minutes to an hour) after eating and felt in 
the epigastrium and back. It may persist for some hours, but is usually 
relieved by vomiting and sometimes by lying in a certain position, e.g., 
upon the left side. It is usually, but not always, made worse by pressure 
upon the epigastrium. 

Vomiting is seen in most cases. It may be severe and constant or 
may occur only infrequently. Usually it takes place an hour or more 
after eating. The vomited matter commonly contains an excessive 
amount of HCl and may contain blood. 

Hematemesis occurs at some time in about one-half of the cases. 
If, as is often the case, the bleeding is profuse, the blood will be vomited 
at once and in an unaltered condition. When the bleeding is slight and 
gradual it may be retained for some time and is then decomposed by 
the gastric juice and when vomited has the brownish black color and 
a grumous consistence which suggest coffee-grounds. The hemorrhage 
may be so severe as to cause death, or frequent smaller hemorrhages may 
result in severe anemia. Often the blood passes through the pyloms 
in quantities sufficient to give the characteristic ''tarry" appearance 



DISEASES OF THE STOMACH 



71 



to the stools. In almost all cases traces of blood may be found in the 
stools by careful chemical tests. 

The DIGESTIVE DISTURBANCES Vary much and include epigastric weight 
and discomfort, acid eructations, nausea, constipation, etc. 

Physical Signs. — Pressure usually reveals a circumscribed area of 
tenderness at some point in the epigastrium and often also a tender spot 
just to the left of the spine and opposite the tenth, eleventh or twelfth 
dorsal vertebra. Rarely the local thickening and induration about an 
ulcer of the anterior surface may be felt through the abdominal wall. 

The CONSTITUTIONAL SYMPTOMS show great variation. In some cases 
the general nutrition and strength are well preserved. In others the 
anemia, wasting and weakness may , be very severe. Fever is usually 
lacking. The gastric contents or vomitus usually show an excess of 
HCl, but normal or diminished acidity does not exclude the presence 
of ulcer. 



Fig. 16. — An oval gastric ulcer showing at its center an eroded artery from which hematemesia 
had resulted. The soft, cloudy appearance is normal to the gastric mucous membrane. From the 
collection of Dr. Walter B. James. 



Course and Complications. — Some of the cases run an acute course 
which may end in recovery or may result in death from hemorrhage 
or perforation. (See Fig. 16.) Occasionally such hemorrhage or per- 
foration may be the first evidence of the disease. In a majority of the 
cases, however, the course is very chronic, the symptoms persisting, often 
with periods of temporary improvement, for a number of years. 

Perforation occurs in about 2 per cent, of the cases. (See Fig. 17.) 
If the ulcer be upon the anterior surface perforation usually results in 
acute general peritonitis. If upon the posterior surface a localized, 
subdiaphragmatic abscess usually follows. Perforation may occur into 
the pleura or pericardium. Pyloric obstruction with secondary dilata- 
tion of the stomach may follow the scarring of a healed pyloric ulcer. 
Adhesive perigastritis is a not uncommon complication. 







72 



DISEASES OF THE DIGESTIVE SYSTEM 



Prognosis. — The mortality varies between 5 and 15 per cent., most 
of the deaths being dne either to hemorrhage or to perforation. 

Diagnosis. — Gastric ulcer may be confused with the gastralgia of 
nervous dyspepsia, with the gastric crises of tabes, with gall-stone colic, 
with gastric, cancer and with hemorrhage from cirrhosis of the liver. 
The characteristic pain (excited by eating and relieved by vomiting^ 
the vomiting, the hyperacidity, the hemorrhages and the prevalence of 
ulcer in chlorotic young women are the features of special diagnostic 
importance. 




Fig. 17. — An old duodenal ulcer showing a perforation from which a subphrenic abscess had resulted. 
From the collection of Dr. Walter B. James. 

Treatment. — The essential feature of this is to give to the stomach 
as nearly complete functional rest as possible. Absolute rest in bed for 
from three to four weeks should be insisted upon. 

Diet. — If the symptoms are severe no food should be given by mouth, 
and rectal feeding should be resorted to for several days at least. (See 
Appendix, p. 587.) When mouth feeding is resumed only the simplest 
food should be given, such as peptonized milk, milk and lime-water, 
albumin-water and meat broths, and these in small amounts frequently 
i-ci)e;it('d. Gradually such articles as junket, meat jelly, custard and gruel 
may be added and later lio-ht and digestible solid food. Proteids, because 
of their tendency to cause free secretion of the acid gastric juice, should 
be used sparingly. 

The Lenhartz diet makes practical application of these principles. 
The feedings are hourly for ten days, then every two hours, except from 
9 P.M. to 7 A.M., during which time they are omitted. Water is given in 
moderate quantities. 



DISEASES OF THE STOMACH 73 



LENHARTZ DIET 



Day 


Egg 


Milk 


Sugar per Day 


Additional Feedings 


1 . . . 


2 cir3,rns 


4 drams 






2. . . 


3 drams 


6 drams 






3. . . 


4 drams 


1 ounce 






4 






O U.id.illb 




5. . . 


6 drams 


1^ ounces 


1 ounce 




6. . . 


4 drams 


2 ounces 


10 drams 


Scraped beef, 3 dr. to each of 3 feedings 


7. . . 


4 drams 


2 ounces 


10 drams 


Boiled rice, 1 dram to each of 3 feedings 


8. . . 


4 drams 


2J ounces 


10 drams 


9. . . 


4 drams 


2 ounces 


10 drams 


Rice, 2 dr. ; dried toast, 5 dr. ; 2 feedings 


10. . . 


4 drams 


2 ounces 


10 drams 


Chicken, 1 ounce; butter, 5 drams 


11. . . 




6 ounces 











Drugs. — Of the many drugs used bismuth subnitrate in large 
doses (5i several times a day) and silver nitrate (gr. ^/4-'%. 
t. i. d.) seem to be the most e^^icacious. Pain is often relieved by alkalies, 
but may require morphine. Vomiting is best treated by withholding 
from the stomach all food for a short time. For hemorrhage, absolute 
rest, morphine and rectal feeding are required. Drugs are of very 
doubtful value in checking hemorrhage. If the anemia is severe, iron, 
arsenic and other tonics are needed. Lavage is usually contra-indicated 
in gastric ulcer. Surgical treatment is indicated (1) for perforation; 
(2) for severe and repeated hemorrhages; (3) in certain chronic cases 
in which pain and other symptoms are severe and show no response to 
medical treatment, and (4) for cicatricial stenosis of the pylorus. 

CANCER OF THE STOMACH 

Etiology. — The stomach is, next to the uterus, the most common 
site of carcinoma. Gastric carcinoma, like other forms, is met with 
chiefly in persons of over forty years, but it is occasionally seen between 
the ages of thirty and forty and, rarely, also before thirty. Men are 
more frequently affected than women. A family history of cancer is 
obtained in a small proportion of the cases, but heredity is certainly 
not an important factor. Alcoholism and chronic dyspepsia also seem 
to have slight if any influence. Occasionally the disease develops in 
the wall of an old gastric ulcer. The cause of cancer is still entirely 
unknown. 

Morbid Anatomy. — The growth may occur at any part of the 
stomach, but in almost two-thirds of the cases it is found in the pyloric 
region. It attacks the posterior surface much more frequently than 
the anterior, and the lesser curvature more often than the greater. In 
8 per cent, of the cases the growth appears in the region of the cardia. 

Varieties. — Four types of carcinoma are met with: the scirrhous, 
the MEDUUUARY or encephaloid, the cylindrical-celled adeno-carcinoma 
and the coiiUOio form. The scirrhous type usually forms a firm, nodular 
mass near the pylorus which frequently causes stenosis; rarely i1 shows 
itself as a diffuse fibrous thickeninii' of the stomach wall ; the medullary 



74 DISEASES OF THE DIGESTIVE SYSTEM 



form and the adeno-carcinoma produce soft, rapidly growing vascular 
tumors which project into the lumen of the organ and tend early to 
break down and to ulcerate; colloid cancer causes a diffuse infiltration 
of all the coats and tends to early involvement of neighboring structures 
with growths of the same gelatinous nature. 

Extension of the disease occurs (1) by the direct involvement of 
adjacent tissues and organs and (2) by metastasis. These metastatic 
deposits occur in a large proportion of the cases and are seen in the 
neighboring lymph-glands, in the liver, intestines, omentum, pancreas, 
lung, etc. 

Secondary Changes. — There is usually a well marked chronic gas- 
tritis. If the pylorus be obstructed marked dilatation of the stomach 
frequently follows. If the growth obstruct the cardia the stomach is 
usually small and the esophagus dilated. Adhesions often occur between 
the stomach and the adjacent organs, and perforation occasionally re- 
sults from extensive ulceration. 

Symptoms. — These are both general and local: 

General Symptoms. — The loss of -flesh is progressive and marked 
(amounting often to 50 or 60 lbs.) and is associated with great loss of 
strength, a waxy pallor and a more or less severe secondary anemia. 
There is often some edema of the legs in the late stages. jModerate fever 
is sometimes seen and there may even be chills. Death occurs usually 
from exhaustion, but it may result from a peculiar type of coma {coma 
carcinomatosum) . 

Gastric Symptoms. — Anorexia is a very constant and persistent 
symptom in most cases and is often accompanied by nausea. 

Pain is present in most cases and is frequently the most troublesome 
symptom. It is usually a more or less continuous dull or gnawing pain 
which lacks the intermittence and the severe paroxj^smal character of 
the pain of ulcer and which bears a less definite relation to the taking 
of food. It may be referred to the epigastrium or to the back or 
shoulder. 

Vomiting occurs at some time in almost all cases. It may appear 
early and be persistent and intractable, or it may occur only in the latter 
part .of the disease and then only occasionally. It is especially trouble- 
some when there is obstruction of either the cardiac or pyloric orifice. 

Hemorrhage. — Blood is found in the vomitus in about one-half of 
the cases. The bleeding is usually small in amount and for that reason 
the blood is retained in the stomach for some time and undergoes chem- 
ical change, so that when vomited it has a dark brown or black color 
and resembles coffee-grounds. Rarely large quantities of bright blood 
may be vomited. If blood reaches the intestine in any quantity it gives 
a black, ''tarry" appearance to the stools. Recently it has been found 
by delicate chemical tests that minute quantities of blood can be demon- 
strated almost constantly in the feces in cancer of the stomach. 

Examination of the Stomach Contents. — Digestion is usually 
slow and imperfect. If there is obstruction at the pylorus stagnation 



DISEASES OF THE STOMACH 



75 



and fermentation of the food may be marked. Fragments of tumor 
tissue, as well as blood, may occasionally be found in the vomitus or 
stomach washings. In the great majority of cases, after a test-meal, 
free HCl is absent and lactic acid is present. Free HCl is occasionally 
found, however, especially in those cases of carcinoma developing upon 
an old ulcer. A very long, non-motile bacillus — the Oppler-Boas bacillus 
— is regularly found when lactic acid is present. 

It has been shown that cancer tissue contains a ferment capable of 
digesting proteids beyond the peptone stage. Upon this fact the glycyl- 
tryptophan test for cancer of the stomach has been proposed. In the 
presence of a peptid-splitting ferment this substance is split into its two 
constituents, glycyl and tryptophan, and the presence of the latter is 
demonstrated by the rose-color produced on the addition of bromide 
water. 

The ordinary Ewald test-breakfast may be employed, or instead white 
bread-toast or biscuit with a glass of sweetened hot water. The test 
requires special training and experience. The presence of saliva, bile, 
or blood may vitiate the test, and its value is still in doubt. 

Physical Signs. — Careful inspection and palpation of the abdomen 
will in many cases reveal the presence of a hard, nodular tumor which 
is usually located in the epigastrium, but may be situated in almost any 
part of the abdomen, and which is often very freely movable. It is 
usually more or less tender on pressure. Peristaltic waves are often to 
be seen and felt. Dilatation of the stomach will give its usual physical 
signs. The liver and subcutaneous lymph nodes should be examined for 
metastatic deposits. 

Complications. — In the majority of cases metastatic growths occur 
in some of the neighboring organs and these, especially when in the 
liver, may give symptoms which altogether mask those of the primary 
disease. The possibility of profuse hemorrhage has been mentioned. 
Occasionally perforation and peritonitis result from ulceration of the 
growth. 

Course and Termination. — The disease usually lasts from six months 
to two years. Acute cases sometimes run their course in three or four 
months. Although quite marked temporary improvement is sometimes 
seen the disease is always fatal. 

Diagnosis. — Chronic gastritis, gastric ulcer, pernicious anemia and 
cirrhosis of the liver are the conditions most likely to be confused with 
gastric cancer. The advanced age, the progressive emaciation, the 
presence of a tumor, the vomiting of blood, the absence of free HCl, 
presence of lactic acid and the absence of characteristic blood changes 
are the features which point most strongly toward cancer. The diag- 
nosis, however, cannot always be made immediately and it occasionally 
happens that the disease runs a latent or masked course throughout. 

Treatment. — Complete removal of the growth by surgical means 
offers the only hope of cure and this is possible only in carefully selected 
cases and when the diagnosis is made very early. Aside from this the 



76 



DISEASES OF THE DIGESTIVE SYSTEM 



treatment is only palliative and symptomatic. Systematic lavage will 
often relieve the dyspeptic symptoms, especially if pyloric obstruction 
exists. The pain may require the use of morphine. The operation of 
gastro-enterostomy, although only palliative, is sometimes of real service 
in the case of pyloric tumors in that it often relieves the pain and the 
tendency to hemorrhage and seems to delay somewhat the growth of 
the tumor. 

ACUTE DILATATION OF THE STOMACH 

Etiology. — While the possibility of acute dilatation of the stomach 
has been known for years, its clinical frequence and importance have 
only recently been recognized. A study of 102 cases by L. A. Conner, 
published in 1907, brought general attention to the subject in this 
country, and led to the more frequent recognition of this condition. It 
has been found in various relations: (1) After operations, particularly 
abdominal operations, under general anesthesia. (2) During convales- 
cence from severe or wasting disease. (3) Following injuries of various 
kinds. (4) After distention of the stomach by large quantities of food 
or drink. (5) In disease of the spine, especially in patients Avearing 
plaster jackets. (6) Without assignable causes in patients apparently in 
good health. 

Morbid Anatomy. — In fatal cases the stomach and the first and second 
portions of the duodenum are greatly distended, the enlarged stomach 
filling the whole left side of the abdomen, and even reaching the pelvis. 
A constriction of the third portion of the duodenum as it crosses the 
vertebrae by the root of the mesentery containing the superior mesenteric 
artery is frequently found. The duodenal obstruction is brought about 
by downward traction upon the root of the mesentery. The gastric 
distention is attributed to the swallowing of air — aerophagia. 

Symptoms. — The clinical picture is that of sudden intestinal 
obstruction, with repeated vomiting of bile-tinged fiuid, abdominal dis- 
tention and tenderness, constipation, thirst, scanty urine, and rapid 
collapse. Any one of these symptoms may be absent. The temperature 
is normal or below, the vomitus is bile-tinged, and may have a foul 
odor, but is not fecal. Distention of the epigastrium and left half of the 
abdomen with tympany, and often splashing sounds or fluctuation below 
the umbilicus, are important physical signs. 

Prognosis. — Of the recorded cases about 75 per cent, proved fatal, 
but doubtless many mild eases recover spontaneously, and prompt rec- 
ognition and proper treatment should insure recovery. 

Treatment. — The stomach should be emptied by the stomach tube, 
and nothing given by mouth for a time. The patient should lie upon 
the abdomen, or upon the right side to relieve the duodenal stricture 
by relaxing the mesentery. Elevation of the foot of the bed may be 
helpful. Feeding by mouth and the oi'diiiary position should be grad- 
ually resumed. 



DISEASES OF THE STOMACH 



77 



CHRONIC DILATATION OF THE STOMACH 
(Gastrectasis) 

Etiology. — Chronic dilatation of the stomach is of two types — 
obstructive and non-obstructive. The obstructive form results from a 
narrowing of the pylorus or duodenum which may be due to such in- 
trinsic causes as cancer, cicatricial stricture of a healed ulcer, sclerotic 
thickening (hypertrophic stenosis), congenital stenosis and possibly 
pyloric spasm; or to such extrinsic causes as the pressure of a tumor, 
peritoneal adhesions, kinking of the pylorus, etc. The non-obstructive 
form results from muscular insufficiency due to habitual over-eating and 
drinking (as in diabetics, beer drinkers, etc.) or to chronic debilitating 
diseases, severe acute diseases (typhoid, etc.) and chronic inflammation 
of the stomach wall. 

Morbid Anatomy. — In the obstructive type there is at first an 
hypertrophy of the muscular coat which may for a time compensate for 
the narrowing of the orifice. Eventually, however, the stomach becomes 
much increased in size and the muscular coat thin and atrophic. The 
mucosa usually shows a well-marked chronic gastritis. 

Symptoms. — These depend upon the imperfect emptying of the 
stomach; the decomposition of the retained food, and the associated 
chronic gastritis. The symptoms develop gradually and consist of a 
feeling of weight and dragging or of dull pain in the stomach, flatulence, 
eructations of gas, and especially the habitUxVl vomiting at longer or 
shorter intervals of very liARGE quantities of fluid and food. In the 
vomited matter there are often to be seen remnants of food eaten many 
hours or even a day or two before. The delay in the emptying of the 
stomach may be demonstrated also by passing a stomach tube before 
breakfast, when food eaten the evening before can be recovered. The 
vomitus has an offensive, sour odor and contains usually a variety of 
fungi and bacteria. The appetite is usually lost, but there may be con- 
stant hunger. The bowels are obstinately constipated, nutrition is usu- 
ally much impaired and, because of the diminished absorption of fluid, 
there are usually thirst, scanty urine and dryness of the skin. Vertigo 
and headache are common. Tetany is an occasional complication. 

Chemical analysis of the stomach contents after a test-meal, and 
of the vomited matter, shows usually great diminution or absence of free 
HCl and the presence of organic acids (lactic, butyric and acetic) due 
to the abnormal fermentative processes. Occasionally HCl may be nor- 
mal or increased in amount. 

The ability of the stomach to empty itself, impaired as a rule either 
by lessened motility of its wall or by ol)stni('ti()n of the pylorus, is most 
simply tested by giving with the evening meal hnlf a dozen raisins or a 
tablespoonful of cranberry or currant preserve. If there is retention, 
the seeds and skins of the fruit will be obtnined on washing out the 
stomach in the morning. 

PiTYRTCATi Signs. — In the dorsal ])()siti()n iNsi'EcrrioN will often show 



78 



DISEASES OF THE DIGESTIVE SYSTEM 



a fullness in the abdomen corresponding to the enlarged stomach, and 
the outline of the greater curvature may be seen lying heloiv the um- 
bilicus (normally it lies a finger's breadth or more above). If there 
be pyloric obstruction waves of peristalsis may frequently be seen pass- 
ing from left to right across the abdomen. By palpation a splashing 
sound is easily elicited even though no food or drink has been taken for 
several hours, and the splash can be produced at points beyond the 
normal limits of the stomach. Pyloric tumors or thickening may be 
felt, and the peculiar elastic feel of the dilated stomach itself may often 
be recognized through the thin abdominal wall. By percussion the out- 
lines of the enlarged stomach may be determined accurately if the organ 
be inflated with, air or gas. This may be done by means of a stomach 
tube and a Davidson 's syringe, or by the use of tartaric acid and sodium 
bicarbonate (aa 3ss-5j) each dissolved in oij of water and taken sep- 
arately. In the erect position the most dependent part of the stomach 
will yield a dull note, from the contained fluid, and this A\all be found 
to be on a level with or below the umbilicus. 

Diagnosis. — For this it is necessary to prove, first, that the stomach 
is enlarged and, second, that food is retained in it beyond the normal 
time (seven hours or less). The condition is to be distinguished from 
an unusually large stomach (megalogastria) in which the motor func- 
tion is not impaired, and which therefore gives no s;vTnptoms; from 
atony of the stomach (as shown by a delay in emptying itself) without 
enlargement, and from gastroptosis in which the stomach is displaced 
and lies abnormally low in the abdomen. 

Radiographic examination of the stomach filled with a bismuth 
emulsion will show its size and position. Retention of the bismuth may 
also be demonstrated by examination 24 hours later. 

Prognosis. — This depends not only upon the nature of the cause, but 
also upon the degree of dilatation and the condition of the muscular coat. 
Non-obstructive cases of moderate severity are often greatly benefited 
or altogether cured by careful treatment. The prognosis of cases with 
non-malignant stenosis of the pylorus has been much improved by the 
recent rapid development of gastric surgery. 

Treatment. — The cause should be carefully sought for and, in so 
far as possible, removed. The diet should be simple and nutritious and 
should be supplied in the form of five or six small meals. Large meals 
and large quantities of fluid are distinctly injurious. 

Lavage is often of very great value. It should be performed daily, 
preferably at bedtime, and may need to be continued for many weeks 
or months. The fluid used may be warm water or some mild alkaline 
or antiseptic solution. 

Hydrochloric acid is often of service in aiding digestion and in 
dim.inishing fermentation. Strychnine and other tonics and abdominal 
massage are of value in improving the muscular tone. 

If marked pyloric obstruction exist little beside palliation can be 
expected from medical treatment and recourse should be had to surgery, 



DISEASES OF THE STOMACH 



79 



which of late has effected many brilliant cures. The relative merits of 
pyloroplasty and gastro-enterostomy cannot here be discussed. 
Gastroptosis. — See Enteroptosis. 



Definition. — Narrowing of the pylorus due to congenital hypertrophy 
of its muscular coats. 

Etiology. — The cause is not known. Sometimes other congenital 
anomalies accompany the pyloric stenosis. Hypertrophy from overwork, 
due either to lack of proper nervous co-ordination or to irritation pro- 
duced by improper food or hyperacidity, has been suggested, but not 
proven. 



Fig. 18. — Hypertrophic pyloric stenosis. Section through the pylorus and adjacent duodenum. 
M, mucous membrane: S M, submucous coat; CM, circular muscular coat; L M, longitudinal 
muscular coat. Dr. John Dorning's case. 



Morbid Anatomy. — The pylorus is found thickened and enlarged, 
often forming a definite tumor, 2 or 3 cm. in length and 1 in width. 
(See Fig. 18.) The lumen is greatly restricted. On section the wall is 
notably thickened by hypertrophy of the muscularis. The other coats 
are normal. The stomach is more or less dilated and consequently 
thinned. 

Symptoms. — These appear within three months of birth. (a) 
Vomiting at first occasionally, later after every feeding, no matter what 
its composition; (b) obstinate constipation, with scanty, hard, dry stools; 

(c) and emaciation are the striking symptoms. Constant crying from 
hunger is naturally common. 

On examination one finds (a) more or less extreme emaciation; (b) 
an abdomen distended, especially in the epigastrium; (c) peristaltic 
waves passing from left to right in the Avail of the dilated stomach; 

(d) possibly a tumor just to the right and above the umbilicus. The 



CONGENITAL HYPERTROPHIC STENOSIS 
OF THE PYLORUS 




80 



DISEASES OF THE DIGESTIVE SYSTEM 



tumor is small, smooth, painless, freely movable; (e) washing ont the 
stomach relieves the distention. 

Diagnosis. — The combination of symptoms and physical signs is 
diagnostic. If no tumor be fonnd, it is possible that the sjnuptoms are 
due to pyloric spasm without hypertrophy and may yield to careful 
feeding and repeated lavage. 

Prognosis is always grave. ]\Iild cases may recover without opera- 
tion, but most require it. 

Treatment. — Careful feeding with a low-fat milk mixture suited to 
the age of the child may be tried. Absolute quiet after feeding is essen- 
tial. Breast-feeding is most favorable, but the time of nursing must be 
limited. 

Lavage, once or twice daily, should be employed. 

Operative relief is usually required and should not be unduly de- 
layed. Gastro-enterostomy, pyloroplasty, and divulsion (Loreta's 
operation) have been tried. The first operation is usually preferred. 

HEMORRHAGE FROM THE STOMACH 
(Gastrorrhagia, Hematemesis) 

Etiology. — Vomiting of blood (hematemesis) may result from bleed- 
ing into the stomach itself {gastrorrhagia) or from the accumulation 
there of blood from some other source, e.g., nose, pharynx, esophagus 
or duodenum. 

Gastrorrhagia may result from (1) Local causes such as ulcer, can- 
cer, traumatism, severe gastritis and miliary aneurisms of the small 
arteries. (2) Passive congestion of the stomach due (a) to cirrhosis of 
the liver; (b) to thrombosis of, or pressure upon, the portal vein; (c) to 
great enlargement of the spleen, and (d) to venous stasis in chronic 
disease of the heart. (3) Changes in the character of the 'blood, as seen 
in such toxic states as yellow fever, small-pox, measles, cholemia and 
phosphorus poisoning, and in such constitutional diseases as the severe 
anemias, leukemia, purpura, scurvy, hemophilia, etc. 

In cirrhosis of the liver a common source of the vomited blood is 
the varicose veins which are so prone to form at the lower end of the 
esophagus. 

Symptoms. — In general the larger the hemorrhage the more 
promptly is it vomited. Rarely even a large hemorrhage may be re- 
tained and passed into the intestine. The vomited blood is usually dark 
colored and more or less clotted. If it has remained in the stomach for 
some time it is apt to have the brownish black, grumous appearance of 
coffee-grounds. Single hemorrhages are sometimes seen, but more fre^ 
quc^ntly the bleeding continues interruptedly for several days or more. 
The symptoms of anemia vary with the severity of the hemorrhage. 

Diagnosis. — Vomited blood is usually readily recognized, but small 
amounts of changed blood may require the aid of the microscope or of 
the chemical or spectroscopic tests. The nose, mouth and throat should 



DISEASES OF THE STOMACH 



81 



be carefully examined for evidence of recent hemorrhage in view of the 
possibility that the blood may have been swallowed. Occasionally it 
may be difficult to decide at first whether the blood has come from the 
stomach or the lungs. In the former case the blood is usually dark 
and clotted, and may be mixed with the acid stomach contents; the 
vomiting usually occurs without cough, the stools may later contain 
blood and there are other evidences of gastric, hepatic or splenic disease. 
In the case of hemoptysis the blood is brought up by coughing, is bright, 
frothy and fluid and is alkaline in reaction. The sputum is subsequently 
blood stained ; moist rales may be heard over some part of the chest and 
there are other evidences of disease of the lungs or heart. 

Treatment. — Absolute rest ; the withholding of all food and drink by 
mouth and morphine subcutaneously are the essential features. Water 
may be given by rectum or by hypodermoclysis. The value of local 
astringents and of ice to the epigastrium is questionable. Stimulant 
drugs, hypodermoclysis or saline infusions should not be used unless 
life is actually threatened by exsanguination. After twenty-four or 
forty-eight hours feeding may be gradually resumed, as in gastric ulcer. 

NEUROSES OF THE STOMACH 
(Nervous Dyspepsia) 

It has been conclusively proved that most of the symptoms of gastric 
disturbance may be produced by purely functional causes and without 
the existence of any recognizable pathological changes in the stomach. 
Such functional disturbances are grouped under the general name of 
nervous dyspepsia and may closely simulate those caused by such organic 
lesions as chronic gastritis, ulcer and cancer. They are seen most com- 
monly in young adults, especially women, and in those of neurotic and 
emotional temperament, and are usually only a part of a general neuras- 
thenia which, however, may be almost altogether masked by the promi- 
nence of the gastric symptoms. 

The gastric neuroses may be sensory, secretory or motor in character. 
These types sometimes occur singly and distinct, but frequently they 
are combined in various ways to make up the complex picture of nervous 
dyspepsia. 

Sensory Neuroses. — (a) Gastralgia ; Gastrodynia. — This neurosis 
presents a very distinct clinical picture characterized by definite parox- 
ysms of intense epigastric pain, lasting from a few minutes to several 
hours, and not accompanied, usually, by vomiting or other gastric dis- 
turbance. The pain may radiate to the back or shoulders and is often 
somewhat relieved by pressure. Following the attack there is frequently 
the passage of a large quantity of pale urine. he attacks usually bear 
little or no relation to the taking of food, but are apt rather to be pre- 
cipitated by such psychical causes as excitement, angei^ etc. The HCl 
of the stomach may be normal or increased in amount. The intervals 
between the attacks vary greatly in length, but often last for months 



82 



DISEASES OF THE DIGESTIVE SYSTEM 



and during this time there are usually no symptoms. Gastric ulcer, gall- 
stone colic, angina pectoris and the gastric pains of tabes dorsalis are 
the conditions most apt to be confused with gastralgia. 

(b) Hyperesthesia of the Mucous Membrane. — Abnormal sensi- 
tiveness of the stomach mucosa to food is the feature of this neurosis. 
This may be shown to all food or only to special dishes. Similar pain, 
burning and distress after eating is seen, of course, in various organic 
diseases and these must be carefully excluded before the diagnosis can 
be made. 

(c) Disturbances of the Appetite. — There may be complete loss 
of appetite {anorexia nervosa), as seen at times in hysteria, melancholia, 
chlorosis, etc.; or abnormally great hunger {hyperorexia, hulimia) ; 
or rarely, the loss of the sense of repletion after eating (akoria). 

Secretory Neuroses. — (a) Nervous Hyperchlorhydria (Hyper- 
acidity). — The secretion of gastric juice containing an excessive amount 
of HCl, which is so constant a feature in gastric ulcer, is seen also as 
a pure neurosis. The symptoms appear usually from one to four hours 
after eating and consist of epigastric pain and burning, acid eructations, 
thirst and often excessive hunger. The pain is usually promptly re- 
lieved by taking of proteid food {e.g., milk) or an alkali, or by 
vomiting. Gastric digestion is prompt and complete. Constipation is 
common. 

(b) Gastrosuccorrhea (Supersecretion) . — In this condition there 
is a more or less constant and abundant secretion of acid gastric juice 
even ivhen the stomach is quite empty of food. It is seen in both a 
periodic and a continuous form. Epigastric distress, burning and pain, 
acid eructations, headache and the vomiting of large quantities of clear, 
yellow, acid fluid are the features. By the use of the stomach tube con- 
siderable quantities of this fluid can be obtained from the fasting 
stomach. 

(c) Nervous Subacidity or Anacidity. — Diminution of the acid of 
the gastric juice is a common manifestation of nervous dyspepsia. 
Rarely there may be complete absence of all gastric secretion including 
the ferments {achyJia ga^trica nervosa). It is characteristic of these 
functional derangements of gastric secretion that the findings of stomach 
analysis are inconstant and varying. At one time there may be diminish- 
ing acidity, at another complete absence of free HCl and at another 
normal gastric juice. 

Motor Neuroses. — (a) Hyperkinesis. Peristaltic Unrest. — 
Excessive muscular activity of the stomach is frequently associated with 
secretory neuroses (hyperchlorhydria, achylia) and occurs rarely as a 
primary neurosis {peristaltic unrest), in which case the active peri- 
staltic movements are felt not only during digestion, but also when the 
stomach is empty. 

(b) Nervous Eructations and Vomiting. — Paroxysms of noisy 
eructation of gas constitute a rather common neurosis of hysterical and 
neurasthenic persons. The gas consists chiefly of air which is uncon- 
sciously swallowed. 



DISEASES OF THE INTESTINES 



83 



Vomiting not due to any organic change in the stomach is seen in 
various affections of the central nervous system (brain tumor, tabes, 
etc. ) , and occurs also as a manifestation of hysteria. 

(c) Functional Disturbances of the Cardia and Pylorus. — Pain- 
ful spasm of the cardia is seen rarely as a primary neurosis. There may 
be insufficiency of the cardia, with the habitual regurgitation of gas or 
food. If the regurgitated food is again masticated and swallowed the 
condition is known as rumination. 

Pyloric spasm, which is so often seen in gastric ulcer, occurs also in 
the purely functional hyperchlorhydria, and in hyperesthesia of the 
mucous membrane. Functional insufficiency of the pylorus, also, is 
recognized. 

Treatment of Neuroses of the Stomach. — Treatment of the under- 
lying nervous state is of primary importance. Rest, out-of-door exercise, 
travel, etc., may be all that is needed in some cases. In others a care- 
fully regulated ''rest cure" may be advisable. Tobacco, alcohol, tea 
and coffee should be used very sparingly if at all. The troublesome pain 
of hyperchlorhydria is best relieved by proteid food and by large doses 
of alkalies — bismuth, magnesia, or sodium bicarbonate. In gastro- 
succorrhea daily lavage, atropine, nitrate of silver (gr. l/4-l^), and the 
alkalies are of value. In the motor neuroses small doses of sodium 
bromide and chloral are often useful. If anemia be present arsenic and 
iron should be used. 

DISEASES OF THE INTESTINES 

I. ENTERITIS 
(Catarrhal Enteritis. Catarrhal Entero-Colitis) 

Inflammation of the intestinal mucosa occurs in both an acute and a 
chronic form, the former being much the more common. 

Etiology. — Acute catarrhal enteritis is of very frequent occurrence 
and may be either primary or secondary. The causes of the primary 
form are: (a) Improper food, such as unripe or over-ripe fruit, tainted 
meat or milk, etc.; (b) violent purgatives and certain mineral and other 
poisons; (c) impure drinking water, and (d) sudden chilling of the 
body and exposure to cold. The secondary form occurs in (a) certain 
infectious diseases, such as typhoid, pneumonia, cholera, etc.; (b) passive 
congestion from cardiac disease or cirrhosis of the liver; (c) various 
cachectic conditions. 

Morbid Anatomy. — The inflammation may affect only a portion of 
the small or the large bowel alone, but as a rule a considerable portion 
of the whole intestinal tract is involved (entero-colitis) . The changes 
are those of catarrhal inflammation of any mucous membrane; 
hyperemia, exudation of serum and leukocytes (swelling) and an in- 
creased secretion of mucus. The h^^;)eremia is rarely apparent after 
death. Swelling of the solitary and agminated follicles is very common, 
especially in children, and the summits of these swollen follicles may 



84 



DISEASES OF THE DIGESTIVE SYSTEM 



become eroded (follicular ulcers). In chronic cases the mucosa may 
be thickened by the formation of new connective tissue or may be 
thinned and atrophic. 

Symptoms. — The disease may be acute or chronic; the former being 
much the more frequent. Diarrhea is usually the chief and sometii:ges 
the only symptom. It is occasionally lacking, however, when the inflam- 
mation is confined to the upper part of the small gut. The stools vary 
greatly in appearance and in number. Their consistence is usually 
watery, the color varies from dark brown to a light yellow or gray, and 
the number from two or three to fifteen or twenty a day. Frequently 
particles of undigested food or shreds of grayish or bile-stained mucus 
are to be seen. Colicky pains and rumbling noises (borborygmi) are 
common and there may be slight general abdominal tenderness. Tenes- 
mus and straining occur when the lower part of the large bowel is 
involved. Fever is slight or lacking. Anorexia, thirst and a coated 
tongue usually accompany the intestinal symptoms. In severe cases the 
prostration is marked and may amount to actual collapse. The duration 
of the acute cases is usually from two to five days. 

Chronic catarrh moj follow an acute attack, may result from 
passive venous congestion or certain stomach derangements, or may 
develop without knoAvn cause. Sharp pain is less common than in the 
acute form, but the nutrition often suffers severely and there may be 
great loss of flesh and strength. Many of the cases are marked by great 
mental depression. Diarrhea occurs often only at certain times of the 
day, e.g., in the early morning or soon after eating. 

Prognosis. — This in the acute cases is uniformly good. Only rarely 
does the inflammation persist and run a chronic course. In the chronic 
form the prognosis is by no means so favorable. Complete recovery is 
not common, although great improvement is often seen from suit^ible 
treatment. Frequently the symptoms persist for many years with alter- 
nating periods of im.provement and exacerbation. 

Treatment. — In the acute cases rest in bed, and a fluid or semi-fluid 
diet should be ordered. If the attack be due to dietetic errors a purge 
of castor oil or calomel should be given at the outset. The pain may be 
relieved by hot applications to the abdomen, spirits of chloroform (oj), 
small doses of opium; or, if severe, by morphine (gr. Vq-V^) subcu- 
taneously. For the diarrhea bismuth subnitrate (gr. xx-xxx), given 
after each loose stool, is usually all that is needed. Treatment of the 
chronic cases is by no means so simple. The cause should be carefully 
sought for and will often be found to lie in some derangement of the 
digestive processes in the stomach. IMuch information may often be 
obtained from careful examinations of the stools for undigested food, 
mucus, pus, blood, etc. In some cases rest in bed for a time and a care- 
fully restricted diet may be all that is required. A strict milk diet is 
beneficial in some, but by no mea.ns in all cases. If the trouble seems 
to lie chiefly in the colon daily large irrigations of normal salt solution 
are often of value. The drugs most frequently found to be of benefit 



DISEASES OF THE INTESTINES 



85 



are the bismuth salts (subnitrate, subgallate and salicylate), given in 
large doses; naphthaline (gr. x-xv), and eapsnles of salol (gr. v), and 
castor oil (TTtv-x). The opium preparations and the strong astringents 
are rarely of permanent benefit. The constant use of a flannel abdominal 
band seems often to be helpful. Some cases are cured by change to a 
warm, dry climate. 

Croupous or Pseudo-membranous Enteritis. — Croupous or diph- 
theritic inflammation of the intestines is seen (a) secondary to certain 
acute infectious diseases, such as pneumonia, typhoid fever, scarlet fever 
and pyemia; (b) as a terminal condition in such chronic 
affections as chronic nephritis, cancer, tuberculosis, cirrhosis of 
the liver, etc., and (c) in poisoning by minerals such as mercury, lead 
and arsenic. The process shows every grade of severity from a thin 
membranous film capping the tops of the folds of the mucosa to an in- 
tense gangrenous inflammation with extensive sloughing. The colon is 
usually the part chiefly affected. The symptoms may be those of a 
severe entero-colitis mth mucus, pus, blood or shreds of false membrane 
in the stools, but frequently the local diarrheal symptoms may be masked 
by those of a severe general infection. 

Phlegmonous Enteritis. — This extremely rare condition usually oc- 
curs as a complication of intussusception, strangulated hernia or intes- 
tinal ulceration. The purulent infiltration involves chiefly the sub- 
mucous layer and may be circumscribed or more or less diffuse. The 
symptoms resemble those of acute peritonitis and usually end fatally. 

CHOLERA NOSTRAS 
(Cholera Morbus) 

Etiology. — This disease is not very infrequent in temperate climates 
during the hot months. It occurs both in adults and in children and 
usually seems to be due to some bacterial toxin formed in tainted meat, 
shell fish, milk, ice cream, etc. In some cases no such cause is discover- 
able. The disease is not transmissible. 

Symptoms. — The symptoms cannot be distinguished from those of 
Asiatic cholera. There is a sudden onset, with persistent vomiting and 
purging ; colicky pains in the abdomen ; cramps in the muscles of the 
legs; great thirst and often alarming prostration. The stools are very 
numerous and soon lose their fecal character, becoming serous and odor- 
less. The attack lasts from a few hours to several days. Complete re- 
covery is the rule. Only rarely does a case prove fatal. The 
post-mortem findings are in no way characteristic. There is usually only 
a moderate grade of catarrhal inflammation of the stomach and intes- 
tines with some swelling of the solitary and agminated lymph follicles. 

Diagnosis. — Confusion with true cholera is not likely unless an 
epidemic of the latter disease prevails. In such cases the differentiation 
can be made only by careful bacteriological examinations of the stools. 
The TREATMENT is similar to that described under Asiatic cholera. 



86 



DISEASES OF THE DIGESTIVE SYSTEM 



II DIARRHEAL DISEASES OF CHILDHOOD 

Etiology. — Age. — Diarrhea is especially prone to attack children 
between the time of weaning and the end of the second year. In bottle- 
fed babies the condition is very common during the first year. 

Season. — Most of the cases occur in hot weather and especially dur- 
ing the months of July and August. The heat seems to exert its baneful 
influence chiefly by favoring bacterial growth and thus hastening fer- 
mentative changes in milk and other foods, rather than by its direct 
effect upon the child itself. The degree of humidity has little or no 
influence. 

Diet. — Diarrheal diseases are vastly more common in artificially-fed 
babies than in those nursed. This is particularly the case among the 
lower classes, where a shocking degree of ignorance and carelessness 
exists as to the selection and preparation of such artificial food. Impure 
or stale milk, unclean bottles and nipples, indigestible articles of food, 
over-feeding and the prolonged use of condensed milk and the various 
proprietary foods are common causes of disease. 

State of Health. — Chronic indigestion, rickets, marasmus, syphilis, 
tuberculosis and all conditions which lower the child's vitality are im- 
portant predisposing causes of intestinal disorders. 

Bacteriology. — Although there can be little doubt that many cases 
of diarrhea in children, especially those occurring during the hot months, 
are instances of bacterial infection, and although the diarrheal stools 
contain many forms of bacteria not found in those of healthy infants, 
the causal relation of a particular organism to any special form of diar- 
rhea has not yet been proven. Bacilli of the colon and proteus groups; 
the pyogenic cocci, and certain saprophytic bacteria such as the hay- 
bacillus, are the varieties usually found. Recently it has been shown 
that the Bacillns dysenterice of Shiga, or an organism very closely allied 
to it, is present in many cases of summer diarrhea of both mild and 
severe type, as well as in certain local epidemics of dysentery in chil- 
dren. Its significance is not yet fully determined. 

CLINICAL TYPES* 

1. Acute Intestinal Indigestion.— This condition regularly results 
from some dietetic error, such as the use of contaminated milk or of 
other improper food. 

The SYMPTOMS depend upon the irritation of the food itself or the 
toxic materials contained in it and not upon any lesion of the intestinal 
mucosa. They usually begin quite suddenly and consist of colicky pains, 
flatulence, diarrhea and more or less constitutional disturbance. There 
may be vomiting. The stools number from four to ten in the 2-1 hours, 
contain curds and other undigested particles, have an acid reaction and 



* The classification of Holt is here followed. 



DISEASES OF THE INTESTINES 



87 



a sour odor and, in infants, are of a green or yellowish-green color. 
Blood is never present and mucus is scanty or lacking. IModerate fever, 
restlessness, and prostration are present at the outset, but usually subside 
within a day or two under proper treatment. I\Iost cases recover within 
three or four days, but in delicate and susceptible children, or in those 
not suitably treated, the condition may be the starting point of some 
more serious intestinal disorder. 

2. Acute Gastro-Enteric Infection (Fermentative Diarrhea). — In 
this form, which prevails in hot weather, the symptoms are manifestly 
due to the absorption of toxic products resulting from abnormal fermen- 
tative processes in the stomach or intestine and not to local inflammatory 
changes, for these are usually slight and insignificant. To this form 
belong a large proportion of the cases of summer diarrhea. Two distinct 
classes of cases are seen : 

(a) Simple Gastro-Enteric Infection. — The symptoms as a rule 
begin quite abruptly with vomiting, diarrhea, colicky pain and a rapid 
rise of temperature to 102°-105° F. In many cases nervous symptoms 
are prominent. There may be great restlessness and irritability or one 
or more convulsions; or, on the other hand, apathy and stupor. The 
pulse is rapid and weak and the prostration sometimes very great. The 
stools number from six to twenty a day. They are at first fecal, but 
soon become thin and fluid and show many undigested lumps of curd 
and fat. A special feature is the very offensive odor of the stools and 
the large amount of flatus which accompanies them. Blood is lacking 
and mucus is present in only small amounts, unless the trouble continue 
for a number of days. I\Iost cases recover within a week or ten days. 
Some few die in collapse and some develop the lesions of ileo-colitis. 

(b) Cholera Infantum. — This term is reserved for an intense and 
virulent form of infection or intoxication which fortunately is far from 
common. It usually attacks debilitated infants and those with existing 
digestive disorders. No characteristic lesions are found in the intestines. 
The clinical picture closely resembles that of true cholera. The onset 
is abrupt with persistent vomiting and purging, the stools being very 
frequent and soon consisting of little but pure serum. They have an 
alkaline reaction and are almost odorless. There is great restlessness or 
stupor, intense thirst, a high internal temperature with cold surface and 
extremities, a grayish pallor, pinched features, sunken eyes and fontan- 
elles, a small and very rapid pulse and profound collapse. Loss of 
weight is extraordinarily rapid and marked. In some cases convulsions 
and symptoms suggestive of meningitis spurious hydrocephalus") 
occur. ]\Iany of the cases die of collapse within the first 24 or 36 
hours; in some others the purging and vomiting cease, but the child 
passes into a state of stupor or coma and dies in the course of three or 
four days; some few recover completely and still others develop the 
symptoms of ileo-colitis. 

3. Ileo-Colitis (Entero-Colitis, Inflammatory Diarrhea). — In this 
type of diarrhea the symptoms are associated with, and depend upon. 



88 



DISEASES OF THE DIGESTIVE SYSTEM 



pronounced inflanmiatory changes in the intestinal mucous membrane. 
Such inflammation may supervene upon any of the forms of diarrhea 
already described or may be primary. The inflammation may be catar- 
rhal, pseudo-membranous or ulcerative. The ulcers may be small and 
limited to the areas about the solitary lymph follicles (follicular ulcers) 
or may be very extensive and deep. The lower portion of the ileum and 
the colon are the parts usually chiefly involved. The severity of the 
symptoms corresponds to that of the intestinal lesions. There is a con- 
tinued fever, loss of flesh and strength, abdominal pain and tenderness 
and diarrheal stools containing much mucus and often' blood and pus. 
In the pseudo-membranous form the stools may contain shreds of false 
membrane. Eectal tenesmus and straining are common and may lead 
to prolapse of the gut. The duration of the disease varies from ten 
days to several weeks. The severest cases are marked by grave consti- 
tutional s\Tnptoms, high fever and death within one or two weeks. ]\Iany 
of the milder cases recover completel3^ but the disease is often very pro- 
tracted and is marked by frequent exacerbations in the symptoms. 
Bronchopneumonia is a common and serious complication. In certain 
of the cases the disease finally assumes a chronic form in which there 
are progressive emaciation, a normal or subnormal temperature, diarrhea 
with mucous stools, t;NTnpanitis and a dry, red tongue. Abdominal pain 
and tenderness are usually absent. Such cases may last for many 
months, but most of them die eventually of exhaustion and malnutrition. 

Prophylaxis — The importance of careful attention to prophylaxis 
can hardly be overestimated since most of the diarrheal troubles in chil- 
dren are preventable. An abundance of fresh air and sunlight, cleanli- 
ness of bodj^ frequent bathing and light clothing in hot weather and 
plenty of pure drinking water are essential to the child's health. Breast 
feeding should be insisted upon whenever possible and weaning avoided 
during hot weather. The importance of the proper selection of artificial 
food, of regularity in feeding, of not overfeeding and of scrupulous 
cleanliness of bottles, nipples, etc., should be impressed upon mothers 
and nurses. Throughout the hot months milk should be sterilized or pas- 
teurized and the drinking water boiled, and in very hot weather the 
quantity and strength of the food should be reduced and an increased 
amount of water given. Evers^ slight digestive ailment demands careful 
attention and the popular notion that in teething infants looseness of 
the bowels is normal and unobjectionable should be vigorously combated. 

Treatment. — In almost every case of diarrhea when seen early there 
are two clear indications — first, to empty the intestines of decomposing- 
and irritating materials and, second, to secure complete rest for the 
digestive oi-gans. The first is best met by the use of calomel or castor 
oil. If tliere is nmch nausea or vomiting calomel is to be preferred. It 
may be given in gr. ^ doses every hour for six or eight doses. The 
second indication is met by withholding all food for 12. 18 or even 24 
hours and relieving thirst by small quantities of water given frequently. 
"When feeding is begun only the simplest foods, such as whey, broths. 



DISEASES OF THE INTESTINES 



89 



albumin-water, malted foods, etc., should be used in small and frequent 
doses. After two or three days milk may usually be begun, but only in 
very dilute form. In most of the mild cases of intestinal indigestion or 
infection little else is required in the way of treatment. In the more 
severe cases the various symptoms may require special treatment. For 
the diarrhea the bismuth preparations — preferably the subnitrate 
(gr. x-xx q. 3^ hrs.) — are to be recommended. The stronger astrin- 
gents and the so-called intestinal antiseptics are usually much less 
satisfactory. If the diarrhea persist and especially if there be much 
colicky pain opium may be needed, but it should always be used with 
caution and should be avoided if possible. It may be given in the form 
of Dover's powder (gr. 1/4~V2)j paregoric (tTtv-xv) or the deodorized 
tincture (TrLi/4-^) every two to four hours. The temperature and the 
nervous symptoms are best controlled by tepid baths or wet packs. If 
stimulation is required brandy (nxx-oss) and strychnine (gr. 1/500- 
1/100) in frequently repeated doses may be used. 

In cholera infantum morphine subcutaneously (gr. 1/100-^1/60) 
should follow promptly after an initial purge of calomel and should be 
repeated once or more if needed to control the purging and to neutralize 
the effect of the toxin upon the heart and nerve-centers. The enormous 
loss of fluid is best met by subcutaneous injections of several ounces of 
normal salt solution. Stimulants should be given hypodermatically and 
the fever controlled if possible by baths and cold water irrigations of 
the colon. Immediate removal of the child to the country or seashore 
will sometimes save an apparently hopeless case. 

In iLEO- COLITIS, in addition to the measures described for gastro- 
intestinal infection, much benefit may be obtained from the daily irri- 
gation of the colon with a large quantity of normal salt solution or some 
mild astringent. Drugs are of little value in these protracted cases and 
the most essential part of the treatment, aside from colon irrigations, 
lies in the careful regulation of the diet. Whenever possible the child 
should be sent to the mountains or seashore. 



INTESTINAL ULCERS 

Ulceration of the intestine occurs in a great variety cf forms. The 
ulcers of typhoid fever, dysentery, tuberculosis, syphilis and cancer are 
described elsewhere. 

Duodenal Ulcer. — This important form of ulcer seems to be identical 
in its mode of origin and its morbid anatomy with the round ulcer of 
the stomach. It occurs almost always in the first portion of the duo- 
denum and within an inch or two of the pylorus. It has occasionally 
developed as a complication of severe bums and of chronic nephritis. 
It is seen much more commonly in men than in women and its period of 
greatest frequency is from the thirtieth to the fiftieth year. 

The symptoms are very similar to those of gastric ulcer, and in many 



90 DISEASES OF THE DIGESTIVE SYSTEM 



cases it is quite impossible to differentiate between the two conditions. 
In general, however, pain is a less constant symptom in duodenal ulcer 
and when present is apt to occur later after meals or when the stomach 
is empty; vomiting is much less common; tenderness also is less fre- 
quent and is usually located in the right hypochondrium ; hematemesis 
is not so often met with, whereas bloody stools (melena) are seen more 
frequently. A good many cases run a latent course and the first indi- 
cation of any trouble may be a profuse intestinal hemorrhage or the 
signs of perforative peritonitis. 

The treatment is that of gastric ulcer, and surgical intervention is 
often required. 

Follicular ulcers are common in the ileo-colitis of children and are 
occasionally seen as a complication to various severe diseases in adults. 
They result from inflammation and erosion of the solitary follicles and 
occur chiefly in the large intestine. 

Stercoral ulcers occasionally result from the irritation of scybalous 
masses in chronic constipation. Such ulcers not infrequently occur in 
the vermiform appendix and seem often to be the starting point of an 
acute appendicitis. 

Solitary ulcers of unlmo\^Ti origin are met rarely in both the 

large and small intestine and may result in perforation. 

Ulcerative Colitis. — Ulcerative inflammation of the colon, quite dis- 
tinct both etiologically and clinically from true dysentery, is not very 
uncommon. It is most often seen in people of middle age. The symp- 
toms are those of diarrhea, pain, slight fever and loss of flesh. The 
stools may contain blood, but mucus is usually lacking, as are also tenes- 
mus and rectal discomfort. The affection often runs a chronic course. 
Treatment is similar to that of dysentery. 

CHOLERA 
(Asiatic Cholera) 

Definition. — An acute infectious disease occurring chiefly in great 
epidemics, caused by a specific micro-organism — the comma bacillus, and 
marked by serous vomiting and purging, painful cramps and collapse, 
and by a very high mortality. 

Etiology. — Cholera is endemic in certain parts of India. From these 
centers it spreads from time to time in devastating epidemics over the 
whole of Asia, to many portions of Europe and occasionally to other 
parts of the world. It has several times visited this country. Infection 
occurs almost wholly through the medium of water (streams, wells, etc.) 
which has become contaminated by the discharges of cholera patients. 
Any derangement of the digestive tract seems to predispose to such in- 
fection. The specific germ is the comma bacillus of Koch, which is 
found in vast numbers in the intestines and stools, but does not occur 
in the blood or viscera. It is a small, comma-shaped, actively motile 



DISEASES OF THE INTESTINES 



91 



organism which enters the g'astro-intestinal tract with the drinking 
water or food and there multiples rapidly, producing at the same time 
a potent toxin to which the violent symptoms seem due. 

Morbid Anatomy. — The body after death has a shrunken, livid look ; 
often there is a high post-mortem temperature. Rigor mortis occurs 
very early and is marked, and post-mortem contraction of the muscles 
is frequently seen. The tissues are abnormally dry; the blood is thick, 
dark and liquid; the intestines contain large quantities of turbid serous 
fluid. The intestinal mucosa is sometimes blanched, sometimes con- 
gested. The solitary follicles and Peyer's patches are swollen and promi- 
nent. The heart, liver and kidneys, especially the last, are apt to show 
extensive parenchymatous degeneration. 

Symptoms. — The incubation period is rarely longer than three or 
four days and sometimes lasts only a few hours. 

It is convenient to divide the symptoms into several stages which are 
more or less distinctly defined. 

1. — The Stage of Preliminary Diarrhea. — In many cases a mild 
diarrhea is present for a day or two before characteristic symptoms 
appear. In other cases the onset is abrupt with 

2. — The Stage of Serous Purging. — There is violent purging. The 
movements soon lose their fecal character and consist of frequent, pain- 
less evacuations of very large quantities of watery fluid containing flakes 
of desquamated epithelium and flbrin — the so-called ' ' rice-water stools. ' ' 
These are odorless and alkaline, are composed of almost pure serum and 
commonly contain neither blood nor mucus. With the purging there is 
usually also persistent vomiting of similar serous fluid. There are intense 
thirst and great restlessness. A striking feature of this stage is the very 
painful cramps, which affect chiefly the muscles of the lower extremities 
and abdomen. As a result of the enormous loss of body fluid there fol- 
lows, usually within twenty-four hours, 

3. — The Algid Stage, or Stage of Collapse. — In this the purging 
and vomiting may cease. The skin is cyanotic and clammy, the cheeks 
and eyes sunken, the voice whispering, the urine, bile and other secre- 
tions are suppressed and the pulse feeble and flickering. The surface 
temperature is much below normal, but the internal temperature is 
usually somewhat elevated. 

If this period is survived the patient may proceed to rapid con- 
valescence, or, after a transient return of warmth, may die in collapse, 
or he may enter 

4. — The Stage op Febrile Reaction. — The purging and abdominal 
cramps subside, the kidneys resume their function, the pulse becomes 
stronger and the body surface warmer, but in many cases the patient 
enters a ''typhoid state" with high temperature, dry brown tongue, 
scanty, albuminous urine, apathy or low delirium, from which he may 
pass to coma and death, or these symptoms after some days may subside 
and the patient enter a slow, tedious convalescence. 

The disease is seen in all grades of severity from the very mild. 



92 



DISEASES OF THE DIGESTIVE SYSTEM 



walking cases to the most virulent type in which collapse and death 
occur within a few hours of the onset. Cholera sicca is a rare and 
rapidly fatal form with little or no purging and vomiting. 

Complications. — These are apt to appear towards the end of the 
disease. Pneumonia, nephritis, uremia, diphtheritic colitis, abscesses, 
local gangrene, parotitis, ulceration of the cornea are all occasionally 
encountered. 

Diagnosis. — The positive diagnosis of sporadic cases can hardly be 
made except by a careful bacteriological examination of the discharges. 
The rice-water stools, the rapid emaciation and collapse and the severe 
muscular cramps are the most characteristic symptoms, but none of 
these is pathognomonic of the disease. The term cholera nostras is 
applied to a form of severe diarrhea occurring in hot weather, which 
may closely simulate true cholera and may even prove fatal. It lacks, 
however, the presence of the specific comma bacillus. 

Acute dj^sentery; the algid form of pernicious malarial fever, and 
poisoning by mushrooms, ptomaines, arsenic, etc., may be mistaken for 
Asiatic cholera. 

Prognosis. — The mortality of different epidemics varies between 
30 and 80 per cent. In general about half of the cases die. The mor- 
tality is usually highest at the beginning of an epidemic. Alcoholism, 
old age, pregnancy, nephritis, debility, etc., are unfavorable features. 

Treatment. — Prophylaxis. — In general this is similar to that de- 
scribed for typhoid fever: protection of the water supply from con- 
tamination b^^ cholera discharges ; the isolation of patients ; careful dis- 
infection of all excreta, clothing, bed linen, etc. ; the boiling of drinking 
water and milk, and the avoidance of everything that will tend to 
derange the gastro-intestinal tract or to lower the general health. Pro- 
tective inoculation of attenuated cultures of the cholera bacillus have 
been used with some success by Haffl^ine in India. 

Treatment of the Attack. — The patient is put to bed at once and 
kept absolutely quiet. The use of a free purge at the beginning of the 
disease has not been found of advantage. The purging, vomiting and 
pain are best controlled by the hj^podermic use of morphine or by 
chlorodyne. No attempt at feeding should be made during the active 
stage. Thirst is relieved by bits of ice or by small quantities of hot 
water. The enormous loss of body fluid is best replaced by the intra- 
venous or subcutaneous injectioji of large quantities of normal (0.8 
per cent.) salt solution. The surface heat should be maintained by 
blankets, hot water bags, etc., or by hot baths. Cardiac stimulants are 
usually needed and should be given hypodermatically in the form of 
strychnine, digitalis, caffeine, ether, etc. After the active symptoms 
have subsided feeding should be begun most cautiously by giving fluids 
in minute (|uantities at frequent intervals. Indeed, throughout the 
whole convalescence the greatest possible care in the feeding is required 
to prevent a return of the purging and vomiting. 



DISEASES OF THE INTESTINES 



93 



DYSENTERY 

Definition. — The term dysentery is applied to inflammatory proc- 
esses of the large intestine, of varied infections nature, characterized 
clinically by the frequent passage of scanty, mucous and bloody stools 
and usually by tormina and rectal tenesmus. 

Etiology. — Dysentery has been known for many centuries as one of 
the great epidemic diseases. It is scattered widely throughout the world, 
but is most commonly seen, and is most severe, in tropical countries. It 
prevails chiefly in summer and autumn and attacks all ages and races. 
It is the scourge of armies in the field and is met with in barracks, jails, 
asylums, etc. It occurs endemically, epidemically and sporadically. 
Infection takes place through the gastro-intestinal tract and usually by 
means of contaminated drinking water. Exposure, fatigue, poor food 
and slight gastro-intestinal derangements are potent predisposing 
causes. 

The classification is still confused and unsettled. The pres- 
ent status of this subject can be understood only by remem- 
bering that until a few years ago all cases of dysentery were classified 
on the basis of the anatomical lesion, as catarrhal, ulcerative, croupous, 
etc. The causative relation of the ameba to certain forms, 
especially of chronic dysentery, was first discovered and recognized in 
the description of amebic dysentery ; later the part of the Shiga bacillus 
was developed, and called for still further changes in classification. 
When the causative agent, ameba or bacillus, can be found, we denomi- 
nate the disease accordingly ; in the absence of such knowledge we must 
fall back on the old anatomical classification. Five types of the disease 
are usually described. (1) Acute Catarrhal, (2) Acute Specific, (3) 
Amebic or Tropical, (4) Diphtheritic and (5) Chronic Dysentery. 

Acute Catarrhal Dysentery. — This is the mildest form and that 
commonly met with in temperate climates, where it occurs sporadically 
and in small local epidemics. It is probable that no single micro- 
organism is responsible for this type of dysentery. ]\Iany cases which 
formerly fell into this class are now known to be due to the bacillus 
dysenterm and to belong, therefore, to the type next to be considered. 

Lesions. — There is an acute catarrhal inflammation of the mucosa 
of the colon and rectum, marked by congestion, increased secretion of 
mucus, excessive desquamation of the epithelium and hyperplasia of 
the lymph follicles. Occasionally small points of ulceration cap these 
swollen follicles. 

Symptoms. — The onset is marked by a diarrhea which is at first fecal, 
but which, within a day or two, assumes a dysenteric character. A chill 
is uncommon. The painless, fecal movements soon change to small, 
mucous, bloody passages containing little or no fecal matter. At the 
same time there are usually severe colicky, abdominal pains (tormina) 
and distressing rectal tenesmus, with constant desire for stool. The 
temperature is usually moderately elevated, and there are increasing pros- 



94 



DISEASES OF THE DIGESTIVE SYSTEM 



tration and loss of weight. The tongue becomes dry and red; the 
abdomen is retracted and often tender. Vomiting may occur. At the 
end of a week or ten days, in most cases, the symptoms subside, the 
stools regain their fecal character and a rapid convalescence is made. 

Of the more severe cases a few are rapidly fatal, but most of them 
run a course of three or four weeks and may then terminate in recovery, 
in death or in chronic dysentery. 

Complications, such as abscess of the liver or intestinal perforation, 
are uncommon in this type. 

Acute Specific Dysentery — Very recently it has been sho\^Ti that 
many epidemics both in the tropics and in temperate regions are due to 
a specific pathogenic micro-organism — the Bacillus dy sentence — discov- 
ered by Shiga in 1898 in the epidemic dysentery of Japan. This germ 
has since been found in a number of small epidemics and in many 
sporadic cases of dysentery both among children and in adults in this 
country and elsewhere. The organism belongs to the colon-typhoid 
group of bacilli, is found abundantly in the stools and intestinal con- 
tents and is to be identified by certain cultural peculiarities. The blood 
of patients suffering from specific dysentery, even when highly diluted, 
agglutinates fresh cultures of this bacillus and this fact has been used 
as an aid to diagnosis similar to the Widal test in typhoid fever. Its 
diagnostic value, however, has not yet been fully determined. 

The LESIONS of specific dysentery are in no wise characteristic and 
vary greatly both in extent and severity. The rectum and sigmoid 
flexure are the regions most commonly affected. Sometimes the whole 
large gut is involved and the process may even extend to the ileum. In 
the mildest cases the lesions are similar to those of catarrhal dysentery. 
More commonly, however, the inflammatory process is more severe and 
is not confined to the mucous coat. The tissues are infiltrated with 
serum, Leukocytes and blood; a grayish pseudo-memhrane, composed 
chiefly of fibrin and the necrosed superficial layers of epithelium, coats 
the inner surface of the gut and this in certain places may separate by 
sloughing and leave idcers of varying depth and extent. 

The SYMPTOMS are similar in kind to those of acute catarrhal dysen- 
tery, but are apt to be more severe. The onset is often violent/ the 
fever high and the prostration extreme. Delirium and coma vigil are 
present in many of the worst cases. The course varies between a few 
days and several weeks. The mortality differs much in different epi- 
demics and is apt to be specially high in the tropics, in crowded insti- 
tutions and among children. "When ulceration is extensive the case is 
apt to be prolonged indefinitely as chronic dysentery. Such complica- 
tions as liver abscess, perforation, peritonitis and septicemia, are occa- 
sionally met with. 

Amebic cr Tropical Dysentery. — A type of dysentery common in 
the tropics, and met with occasionally in this country and in other 
temperate regions, is that constantly associated with the presence in the 
intestines of an ameba which is believed to be its specific cause. This 



DISEASES OF THE INTESTINES 



95 



Ameha dysenterim is a large oval, unicellular organism with active 
ameboid movements and phagocytic action. It is found in great num- 
bers in the freshly passed mucous stools and is present also in the 
inflamed intestinal walls and in the pus and walls of the commonly 
associated liver abscess. The amebae are best detected by their ameboid 
movement. To this end the mucous parts of the stool should be placed 
on a warmed slide and examined microscopically immediately after being 
passed. 

The LESIONS of amebic dysentery are quite characteristic and differ 
much from those of other types. The essential change is a peculiar 
gelatinous infiltration and transformation of the submucosa with idcera- 
tion of the overlying mucous membrane. The lesions are confined 
usually to the colon and rectum. The ulcers are of various shapes, with 
ragged and undermined edges. The changes in the submucosa are usu- 
ally much more widespread and severe than the extent of the ulceration 
would indicate. In long-standing cases there is often much connective 
tissue proliferation which may result in great thickening of the wall of 
the gut and narrowing of its lumen. A secondary lesion of much im- 
portance is that of abscess of the liver. The abscess is usually, but not 
always, single. The material from such abscesses consists chiefly of 
.broken-down liver cells, fat droplets, granular detritus and amebse, with 
little or no true pus. 

Symptoms. — The course of the disease is usually subacute or chronic, 
although the onset may be sudden and the symptoms at first severe. 
There are prone to be periods of exacerbation and remission. Pain and 
tenesmus are less constant than in the other types of dysentery^ and the 
stools are by no means always mucous and bloody. The temperature is 
usually not much elevated, but there are progressive weakness and emacia- 
tion. In the chronic cases periods of constipation alternate with those 
of diarrhea. Abscess of the liver is a common and grave complication. 
Intestinal perforation is sometimes met with. Death may occur from 
the severity of the early symptoms, from exhaustion or from abscess 
of the liver. 

Diphtheritic Dysentery. — This term is applied to eases of colitis in 
which the inflammation is of diphtheritic or pseudo-membranous type. 
Some of these cases no doubt belong in the class of acute specific dysen- 
tery. The whole, or a considerable part, of the large intestine is the 
seat of a severe exudative inflammation with the formation of a necrotic 
pseudo-membrane which, in places, sloughs off and leaves areas of ulcera- 
tion. In the severest cases the whole inner surface of the colon is a 
black, stinking, gangrenous mass. 

Primary cases usually run a severe course and are very fatal. The 
dysenteric symptoms are often obscured by the severity of the constitu- 
tional symptoms and the condition is frequently mistaken for typhoid 
or for septicemia. 

Secondary cases are occasionally met with in lobar pneumonia and 
in the chronic and wasting diseases, such as chronic nephritis, chronic 



96 



DISEASES OF THE DIGESTIVE SYSTEM 



heart disease, tuberculosis, etc. The condition is frequently overlooked; 
the symptoms being masked by those of the primary disease. 

Chronic Dysentery. — This may follow any of the above described 
forms. Ulceration, scarring, thickening of the submucous and muscular 
coats and polypoid outgrowths of the mucosa are the common lesions. 
The intestinal symptoms vary much from time to time. Diarrhea alter- 
nates with constipation and there is usually great loss of flesh and 
strength. The course of the disease is very long and tedious. A com- 
plete cure is difficult to obtain and many cases eventually die of exhaus- 
tion and malnutrition. 

Treatment of Dysentery. — In all acute cases absolute rest in bed is 
required. If seen at the outset the patient should be given a purgative 
dose of Rochelle salts or castor oil. It is essential that the inflamed 
colon be given as nearly complete rest as possible. With this in view the 
food should be such as will be easily digested and will leave as little irri- 
tating residue as possible. Milk, whey, egg-water or broths should be 
given in small amounts and at short intervals. The pain and tenesmus 
are best controlled by the subcutaneous use of morphine or by rectal 
injections of starch-water and laudanum. Hot poultices or stupes to 
the abdomen are often grateful. The use in acute cases of astringent or 
antiseptic drugs internally is of somewhat doubtful value. Bismuth in 
very large doses (oss-gj per diem) is often useful. In the tropics 
ipecacuanha, in a single very large dose (gr. xxx), has long been a 
favorite remedy. In the subacute and chronic cases irrigation of the 
colon with large quantities of a weak astringent solution (nitrate of 
silver, gr. xv-xxx to a pint) is often of great value. In amebic dysen- 
tery colon irrigations of a solution of quinine (1 to 5000 to 1 to 1000) 
are recommended. In chronic dysentery care must be taken that 
strength is maintained by a diet which is nutritious as well as bland 
and unirritating. In cases hopelessly chronic the operation of right 
inguinal colostomy is justifiable and has sometimes resulted in complete 
cure. Irrigation of the colon through the appendix, which has been 
brought up into an abdominal incision and then opened (appendicos- 
tomy) has also been practiced with success. Finally complete removal of 
the colon has been done in a few cases. In acute specific dysentery the 
serum of animals immunized to bacillus dysenterice has already been 
used with some measure of success. 

APPENDICITIS 

Definition. — An inflammation of the vermiform appendix. 

Etiology. — The disease occurs at all periods, but is most common 
between the ages of 10 and 30. It is uncommon but not unknoA\Ti in 
infancy and old age. Males are affected two or three times as often as 
females. 

Local conditions of the appendix are important. (a) Conditions 
favoring the retention of fecal contents, such as stenosis of the month 



DISEASES OF THE INTESTINES 



97 



of the appendix, either of the so-called valve of Gerlaeh or the adjacent 
portion of the tube, (b) Fecal concretions or foreign bodies of any 
kind. Parasites, particularly the oxyuris vermicularis, pins and fecal 
concretions are not infrequently found in the appendix. These foreign 
bodies, by injury of the mucous membrane, appear to open the way for 
the invasion of the micro-organisms present. 

Bacteriology. — The infection is nearly always mixed, the bacillus 
coli being found with other organisms: streptococci or staphylococci, 
bacillus lactis aerogenes, bacillus aerogenes capsulatus, bacillus pyocy- 
aneus and various other organisms of those which may be found in the 
intestine. 

Morbid Anatomy. — Acute Appendicitis. — The anatomical changes 
vary from the mildest type of inflammation (catarrhal) to the severest 
forms (suppurative or gangrenous). In the milder types the changes 
may be very slight, simply congestion and slight swelling of the several 
coats, in the latter the whole appendix may be destroyed with the de- 
velopment of an abscess or a general suppurative peritonitis. The 
inflammatory changes affect the contents of the appendix, the walls 
of the appendix, and the surrounding tissues. 

Contents. — These may consist of normal feces, of a fecal concretion, 
a foreign body, or of an inflammatory exudate comprising mucus, or 
blood, or pus, of varying consistency. The exudate, especially if the 
mouth of the appendix be closed as the result of deformity or of the 
inflammatory changes, may distend the appendix sufficiently to aid in 
or cause its rupture. In severe cases the contents of the appendix have 
the foul odor usually found in colon bacillus infections. 

Walls of the Appendix. — The coats of the appendix may be slightly 
thickened by the exudate or they may be considerably increased in depth. 
Often more or less necrosis of tissue is present at a localized area, pro- 
ducing an opening (perforation) through which the contents escape, or 
a widespread destruction of the organ, so that at operation only the tip 
or the stump or no part of it may be discoverable. About the area of 
perforation the adjacent tissue is commonly black, necrotic and foul- 
smelling. 

Siirroiinding Tissues. — The peritoneal coat of the appendix may 
show no changes in the very mild eases, or it may be simply congested, 
or it is the seat of an acute fibrinous, suppurative, or gangrenous inflam- 
mation. Corresponding changes occur in the abdominal peritoneum 
and it may be simply congested or the seat of a general suppurative or 
gangrenous inflammation. If, however, as often happens, the appendix 
is shut off by adhesions, an abscess cavity forms about the appendix 
(localized suppurative peritonitis) containing pus, possibly blood and 
the remains of the appendix. 

Suppurative inflammation, either localized or general, usually re- 
sults from perforation of the appendix, but may develop without definite 
perforation, the infecting organisms making their way through the in- 
flamed wall of the organ. The abscess may lie in the pelvis, in the right 
7 



98 



DISEASES OF THE DIGESTIVE SYSTEM 



iliac fossa, in the loin behind the ceciim or colon, or indeed in any part 
of the abdominal cavity. 

Remote Lesions. — The suppurative inflammation may produce throm- 
bosis of radicles of the portal vein. If these break down secondary 
pylephlebitis or multiple pyemic abscesses of the liver may result or 
an abscess may form retroperitoneally (subphrenic, etc.). Pulmonary 
infarction or thrombosis occasionally folloAvs appendicitis, seemingly 
from the dislodgment of a local thrombus in the appendix area. 

Chronic Appendicitis. — As the result of one or more attacks of acute 
inflammation, especially of the mild character usually termed catarrhal, 
the walls of the appendix may become very much thickened, its lumen 
narrowed and distorted and the organ surrounded by dense adhesions. 
In some instances the canal of the appendix is obliterated and the ap- 
pendix is reduced to a dense mass of fibrous tissue (obliterative appen- 
dicitis). To these results of repeated attacks of acute inflammation 
which often constitute a more or less chronic process, the term chronic 
appendicitis is applied. 

Symptoms. — The symptoms of acute appendicitis must vary with 
the severity of the attack. In any event they are both general and local. 
Pain, usually severe, referred at first to the epigastrium or the abdomen 
generally and after an hour or two located in the right iliac fossa, or 
over the situation of the appendix, if it be situated elsewhere (the right 
hypochondrium or the left side of the abdomen), marks the onset. With 
the pain, nausea, vomiting, a rising temperature (102°-103°) and con- 
stipation are regularly associated. In rare instances diarrhea occurs. 
The prostration varies with the degree of fever and the severity of the 
pain, but profound prostration may accompany gangrenous inflammation 
with, little fever. 

Physical Signs. — At the onset there is indeflnite abdominal tender- 
ness, later tenderness to pressure in the right iliac fossa, often sharply 
localized over the base of the appendix at a point mid-way between 
the umbilicus and the anterior superior spine (McBurney's point), with 
definite rigidit}^ of the muscles of the abdominal wall of the right lower 
quadrant of the abdomen. If the appendix is abnormally situated the 
local signs are accordingly misplaced, so that they may be found at 
any part of the abdomen. 

Course and Later Signs. — 1. Resolution. — In the mild cases the 
pain subsides after 24 or 48 hours, the temperature falls, the pulse 
returns to normal, and the local signs disappear. In severer cases the 
fever, nausea, vomiting, and pain persist, the prostration is marked, the 
local signs continue, become more and more marked and the condition 
terminates in a localized abscess about the appendix or in acute general 
peritonitis, or resolves after several days' severe illness. 

Abscess Formation. — IMore or less local peritonitis commonly accom- 
panies appendicitis. In acute inflammation, if the local peritonitis walls, 
off the appendix from the general peritoneal cavity and the inflammation 
continues, a peri-appendicular abscess is produced. Fever continues as 



DISEASES OF THE INTESTINES 



99 



a rule, although an abscess may develop with a falling temperature, 
and the temperature runs the irregular course of septic inflammation. 

The pulse remains more or less rapid, the prostration continues, 
vomiting may be repeated, sweating may occur, and in protracted cases 
the patient loses flesh and becomes anemic. The local signs become more 
and more marked, the tenderness and rigidity persist and resistance in- 
creases in the right iliac fossa, and after a time dulness and a definite 
tumor may be made out in this region. Fluctuation can rarely be 
determined. If the abscess be pelvic, the right iliac fossa may present 
little or no abnormality, and the pain, tenderness and tumor may be 
detected only by rectal examination. Similarly the signs of abscess may 
develop in the hypochondrium or other part of the abdomen. If opened 
and drained, the temperature gradually falls, the abscess closes after 
two or three weeks, and recovery ensues. Unopened, such abscesses may 
possibly rupture through the abdominal wall, in the thigh below Pou- 
part's ligament or in the loin, but such results are not seen under 
modern surgical practice. Acute general peritonitis may develop from 
rupture or extension of inflammation from such an abscess. 

Acute General Peritonitis. — This usually results from the severer 
types of infection and inflammation, but it may follow apparently mild 
attacks. Its development is usually gradual and marked by steadily 
progressive increase in both constitutional and local symptoms. It may, 
however, develop suddenly and unexpectedly in any case of appendicitis. 
Y\^ith the onset of acute general peritonitis the fever continues and 
usually rises, the pulse becomes more rapid, the vomiting more frequent, 
the prostration more profound, so that the facies becomes "pinched " 
and often ashen. Locally the abdomen becomes distended, painful, tender, 
and rigid in all parts, and the illness runs the course of acute general 
peritonitis from any cause (see page 143). Unless relieved by operation 
death is inevitable within a few days. 

Special Symptoms. — Head's zones — cutaneous hyperalgesia. Hyper- 
sensitiveness of certain definite areas of the skin has been found to 
be associated with disease of the viscera. The areas thus affected are 
definite and fairly fixed and their demonstration is helpful in the recog- 
nition and differentiation of \^sceral affections. The cutaneous hyper- 
algesia is demonstrated by pinching the skin or lightly and evenly 
stroking it with the point of a needle, first from side to side and then 
from above downward, the patient reporting whenever the sensation 
becomes painful and the point thus indicated being marked. In the 
case of appendicitis the area thus outlined is found to cover the right 
half of the abdomen below the level of the umbilicus and not quite 
reaching Poupart's ligament, an area corresponding to the right 10th 
and 11th spinal segments. 

The Blood. — A definite leukocytosis is regularly present, 12,000 to 
15,000 or more, and in the severest cases the count often exceeds 30,000. 
Similarly there is an increase in the percentage of polynuclears above 
the normal of 75 per cent., and sometimes amounting to 90 per cent, to 



100 



DISEASES OF THE DIGESTIVE SYSTEM 



95 per cent, of the total amount. In a general way these two reactions 
are associated, the higher the leukocytosis, the more likely the polynuclear 
percentage is to be increased, and as a rule they correspond to the 
severity of the attack. Thus the mild attacks show little or no leuko- 
cytosis and a normal polynuclear percentage ; the severe cases usually 
show high total counts and high polynuclear percentages. ]\Iany excep- 
tions to these rules are observ^ed, and it is quite possible that an acute 
appendicitis with perforation of the appendix and beginning acute peri- 
tonitis should show a low leukocyte count and no disturbance of the 
ratios. The blood reaction should be regarded as one of the symptoms 
of the disease and valued accordingly. 

Chronic Appendicitis. — Two types are recognized. 

1. Persistent local tenderness and constipation with more or less 
intestinal indigestion, shown by nausea, tympanitic distention and a 
coated tongue, mark the first type. 

2. The second type is marked by recurrent brief attacks of pain, 
tenderness and rigidity in the right iliac fossa without constitutional 
disturbance, or by frank attacks of acute appendicitis. Any one of these 
attacks may develop into severe appendicitis with abscess formation or 
general peritonitis as a sequel. These cases are frequently mistaken for 
gastric ulcer or for gall-stones. 

Diagnosis. — An acute inflammatory condition of any of the abdom- 
inal viscera may give the same general symptoms as acute appendicitis, 
especially affections of the stomach, gall-bladder, right kidney, and the 
tube and ovary of the right side. For differentiation we must depend 
largely upon a knowledge of a cause for such disease, of previous dis- 
ease of one of these organs, the location of the pain and physical signs, 
and the relative frequency of acute appendicitis. Attacks of acute 
appendicitis, moreover, regularly occur without apparent exciting cause. 

Perforating gastric or duodenal ulcer gives a history of previous gas- 
tric indigestion, or possibly hematemesis, and the local signs are found in 
the epigastrium or the left hypochondrium. 

Acute cholecystitis or cholangitis follows gall-stones or jaundice or 
develops in the course of typhoid fever or pneumonia, and the local 
signs center in the right hypochondrium adjacent to the 9th costal 
cartilage. 

Acute pyelitis or abscess of the kidney is indicated by previous his- 
tory of genito-urinary infection, urethritis or cystitis, by the presence 
of pus or blood in the urine and local tenderness in the Hank as well as 
in the abdomen. 

Renal or uteral (right) colic may closely simulate acute appendicitis, 
but the presence of blood in the urine and the results of X-ray examina- 
tion are decisive. 

Dietl's Crises, due to floating kidney, should be recognized by the 
demonstration of the presence of a movable organ. 

In women acute inflammations of the right appendages (tubes and 
ovaries) are often mistaken for api)endieitis. A history of previous pel- 



DISEASES OF THE INTESTINES 



101 



vie disease (vaginitis or endometritis, pelvic cellulitis) is helpful and 
the location of the local pain, tenderness and rigidity in the groin and 
the results of vaginal examination are important. 

Acute enteritis arises from definite cause, overfeeding or improper 
food, as a rule, is accompanied by little fever, and free diarrhea, and 
the local signs are centered about the umbilicus. 

]\Iucous colitis gives rise to attacks of pain, fever and constipation, 
easily mistaken for acute appendicitis. The disease belongs especially 
to neurotic women and a history of previous attacks with the passage 
of large quantities of mucus can be obtained. 

Typhoid fever may begin with such acute abdominal symptoms as to 
suggest appendicitis. The history of several days' illness before coming 
under observation, the headache, insomnia and prostration, diarrhea if 
present, and the low leukocyte count, the enlargement of the spleen, and 
possibly the roseola should indicate the correct diagnosis. 

Pneumonia, especially in the young, may begin with abdominal 
pain, tenderness and -rigidity, very suggestive of appendicitis. 
Very high fever, rapid respiration, cough or expectoration should excite 
suspicion, and careful physical examination v/ill usually elicit signs of 
dry pleurisy or consolidation. Several days' observation may be re- 
quired to settle the question. 

Prognosis. — While it is true that even the mildest cases of appen- 
dicitis may be complicated by serious conditions, even general peri- 
tonitis, as a rule those with mild symptoms at the outset remain mild 
and recover promptly. In the severer cases prognosis is always difficult 
because of the dangers of localized peritonitis or abscess, or acute gen- 
eral peritonitis, and the possibility of later disturbances. The mortality 
of cases of appendicitis not operated upon lies between 5 and 10 per cent. 

Treatment. — Absolute rest and quiet are essential. The patient is 
put to bed, the bowels emptied by a high enema or by a mild purgative, 
such as castor oil or calomel. Many object to the use of purgatives in 
appendicitis, but their reasonable use does no harm. All feeding should 
be stopped and only water or cracked ice allowed by mouth. For the 
relief of pain heat by the hot water bottle, poultice or hot fomentations, 
or an ice-cap may be employed. Opium or morphine must be employed 
if the pain is intense, but should be given in small doses, as undoubtedly 
large doses of opiates benumb the patient's senses and mislead the 
physician as to the true conditions. 

Mild cases improve promptly and usually are well in a few days. 
Feeding is resumed as the symptoms subside. 

Immediate surgical intervention is advised by some for all cases, 
and is certainly to be recommended for all beginning severely or becom- 
ing more severe after the onset. Surgical advice should therefore be 
had in all such conditions. As a rule the early operations ;iro the safest, 
and only under special conditions is operation delayed, when deemed 
necessary. Even when acute general peritonitis has developed many of 
the patients are saved by surgical treatment. 



102 



DISEASES OP THE DIGESTIVE SYSTEM 



INTESTINAL OBSTRUCTION 
(Ileus) 

Etiology. — Intestinal obstruction is produced by a variety of 
mechanical conditions which block the intestine and stop the normal 
progress of the contents. The symptoms of obstruction are explained 
first by the failure of the normal evacuations (constipation, more or 
less absolute), and secondly by a reverse peristalsis which develops in 
the portion of the intestine above the block and empties it by discharging 
the contents into the stomach, from which they are ejected by vomiting. 

The causes of obstruction may be classified thus: 

1. Strangulation, the constriction of the bowel in one of the many 
hernial pockets of the abdomen, or by bands or cords, such as peritoneal 
adhesions, Meckel's diverticulum, the remains of the vitelline duct, or 
an appendix adherent by its tip alone. The numerous fossae formed by 
the peritoneum (twelve are described) may, any of them, be the site of 
strangulation. One-third of all cases of obstruction are produced in 
this manner. Males are more often affected, especially in the years from 
15 to 30. The obstruction is nearly always in the small intestine. 

2. Invagination, the telescoping of one part of the intestine into 
another. One part of the intestine becomes unusually contracted by 
excessive peristalsis and the portion below is then drawn upward over 
it. The process regularly begins at or near the ileocecal valve, and the 
invaginated portion may be carried downward through the colon and 
rectum till it presents at the anus. (See Fig. 19.) 

Invagination occurs especially in infants under one year, but may 
occur in children up to the tenth year. It is unkno^^Ti in later life. 
This process also accounts for about one-third of all cases of obstruction. 

As a result of invagination a tumor is formed, composed of the two 
tubes of intestine, one inside of the other, and the mesenterj^ of the 
telescoped portion. The latter portion is spoken of as the intussus- 
ceptum, the outer tube as the intussuscipiens. This included part be- 
comes intensely congested and hemorrhages of some amount occur from 
the engorged mucous membrane. Recovery may occur normally either 
by release of the intussusceptum and return to natural relations, or by 
the sloughing off of it with union of the intestinal walls at its base. 
Fibrous stricture at the point of juncture may result. 

3. Twists (volvulus) and Knots. — These occur in nearly all cases in 
the sigmoid flexure, near the rectum. The bowel may be twisted on its 
long axis, a half or whole turn, producing complete strangulation. 
About 14 per cent, of cases of obstruction are thus explained. This 
condition belongs to adults, 30 to 40 years of age, especially men. 

4. Strictures and Tumors. — Congenital stricture by malformation, 
such as imperforate anus, is well known. In later life strictures result 
from the healing of ulcers, syphilitic, stercoral, or tubercular, dysen- 
teric, or typhoid, or from localized peritonitis. Tumors of the intestine 



DISEASES OF THE INTESTINES 



103 



may obstruct its lumen by growth, or the obstruction may be caused 
by the pressure of tumors in other organs, such as uterine fibroids. 

Cancer, especially in women over 40, is the most common, but all 
manner of tumors have been found. Among the rare forms to be men- 
tioned are papilloma, fibroma, adenoma, or lipoma. 

5. Abnormal Contents. — Gall-stones and fecal impaction are the com- 
mon forms. Gall-stones are seen especially in women over 50. Fecal 
impaction may occur in either sex at any age. Enteroliths may be 




Fig. 19 — An ileocolic intussusception. Small intestine above; colon below. Apex of intussus- 
ception swollen, congested and covered with membranous exudate. Appendix in upper left-hand 
corner. 



formed with bits of bone, masses of hair or other foreign substance as 
a nucleus. They may have become large enough to obstruct the bowel. 
Foreign bodies may be swallowed or introduced into the rectum and 
eventually give rise to obstruction, although the great majority are 
regularly passed without harm. 

Peritonitis. — In any form of intestinal obstruction a localized peri- 
tonitis is likely to develop at the site of the obstruction. Especially in 
strangulation, intussusception ami volvulus, in whieh gangrene of the 



104 



DISEASES OF THE DIGESTIVE SYSTEM 



bowel occurs, the peritonitis may become general and the clinical picture 
gradually changes to that of acute general peritonitis. 

Symptoms. — These include (1) pain, (2) constipation, more or less 
absolute, (3) vomiting, persistent, (4) tympanites, and possibly (5) 
tumor. 

The PAIN is at first colicky, later continuous. It may be referred to 
the seat of obstruction or be general. Localized tenderness may be 
present, but is more often not observed. 

CoxsTiPATiox may be marked from the beginning or the contents of 
the bowel below the obstruction may be passed at first with no subse- 
quent evacuations. In intussusception, however, the engorged intus- 
susceptum may discharge blood and mucus, which are passed in frequent 
small stools, at times suggesting dysentery. In complete obstruction 
of the bowel not even gas may be passed by rectum. The vomiting is 
produced by reverse peristalsis, emptying the bowel, so we see in suc- 
cession stomach contents, bile-stained (green) fluids from the duodenum, 
then the contents of the lower intestine which gradually assume the 
character and odor of fluid feces. These changes in the nature of the 
vomited material may be shovTi in the course of 24 hours, but the 
so-called fecal vomiting is usually seen at the end of the second or third 
day. 

Tympanites is produced by the distention of the portion of the 
bowel above the obstruction. It is more marked the loAver the site 
of the lesion. The pattern of the distended intestines sho^^Ti through 
the abdominal wall may therefore be of help in determining this point. 
If the obstruction is in the upper part of the intestinal tract there may 
be little distention, or the t^Tnpanitic area may be limited to the stomach 
and adjacent portion of the duodenum. 

A palpable tumor is most often found in cases of intussusception. 
It then has a very suggestive sausage shape and feeling. Tumors may 
also be met with in the case of new gro\Al:lis either in the wall of the 
intestine or, in cases where the obstruction is produced by pressure from 
without, in other abdominal viscera. As already noted, in intussuscep- 
tion the tumor may also be felt by rectal examination. Fecal impactions 
may be made out by either abdominal palpation or rectal examination, 
or both. 

Constitutional symptoms are usually slight at first but rapidly 
become marked. Fever is absent at the onset, but after the fii'st day 
the temperature either shows a slight rise or becomes subnormal. It may 
remain below normal throughout. The advent of peritonitis is marked 
by a rise of temperature and characteristic local signs. Owing to the 
persistent vomiting there is great thirst, and the urine is scanty and 
liigli-colored. The urine may show albumin and casts and may contain 
much indican. Prostration is regularly marked from the beginning. 
The pulse, at first but little affected, regularly becomes rapid and weak. 
T^'nless the obstruction is relieved the patient succumbs from exhaustion 
or from peritonitis in from three to six days. 



DISEASES OF THE INTESTINES 



105 



Chronic obstruction is most often seen as the result of stricture, 
either simple or malignant, or fecal impaction. In these cases there is 
a history of repeated attacks of obstinate constipation with abdominal 
pain and distention and nausea or vomiting, each attack becoming 
severer than the preceding one and being relieved with greater diffi- 
culty, till one ends in the picture of complete and permanent obstruction. 

In cases of fecal impaction the bowel may be enormously distended, 
its wall eroded and even perforated without the production of complete 
obstruction. After a period of constipation there may be diarrhea, the 
fecal mass in some cases being channelled so as to permit the passage 
of fluid material from above. The fecal tumor may be located by 
abdominal examination or exploration of the rectum. It is usually of 
large size, has a characteristic doughy feeling and can be indented by 
the fingers, and is painless. 

With simple or malignant stricture there is the same history of in- 
creasing difficulty in securing evacuation of the bowels, with attacks of 
partial obstruction from time to time. Finally the obstruction becomes 
complete and the symptoms are those of acute obstruction, but the 
progress of the affection is usually slower than in the other types of 
that condition. In elderly people with malignant stricture there may be 
emaciation and anemia, but it is not uncommon to see carcinoma produce 
local obstruction without constitutional symptoms. 

Diagnosis. — The onset of the symptoms enumerated without fever, 
and the gradual change in the nature of the vomitus are characteristic 
of intestinal obstruction. We must, however, exclude the presence of 
certain acute inflammatory processes which may give a similar picture. 
Appendicitis is differentiated by early fever and rapid pulse, and the 
local pain, tenderness and rigidity. The bowels respond to enemata. 
Peritonitis also begins with febrile s^Triptoms, general and exquisite pain, 
tenderness and rigidity. The vomiting of peritonitis resembles that of 
obstruction, but never becomes truly fecal. Pancreatitis (acute hemor- 
rhagic) may readily be mistaken for intestinal obstruction, but is usually 
recognizable by early febrile symptoms, the extreme pain, tenderness, 
distention and rigidity in the epigastrium without the vomitus char- 
acteristic of obstruction. Having excluded these possibilities we must 
seek to determine the site and nature of the obstruction. 

The Site. — The higher in the intestinal tract the obstruction occurs, 
the earlier and more severe the vomiting, and the earlier will collapse 
appear, and the less the general abdominal distention. The lower the 
location of the obstruction, the slower the evolution of the symptoms 
and the more marked the distention. The outlines of distended intes- 
tines may indicate the site of obstruction. Thus in low obstruction the 
colon will stand out prominently. With the lesion near the ileocecal 
valve, the distention is mainly about the umbilicus and the colon is flat. 
With high obstruction only, the stomach and adjacent parts of the 
intestines will be distended. The location of a tumor or mass in the 
abdomen or pelvis may be conclusive as to this point. 



106 



DISEASES OF THE DIGESTIVE SYSTEM 



Nature of Obstruction. — The age and sex of the patient are im- 
portant, as already indicated. In children intussusception is by all 
means the most frequent form, in adults strangulation. All accessible 
sites of hernia must be carefully examined, remembering that we have 
no means of detecting hernia into any of the peritoneal fossae men- 
tioned above. Knowledge of a previous peritonitis or previous abdominal 
operation, either of which may leave adhesions, is helpful. Such condi- 
tions are naturally most frequently met with in women. In men over 
forty volvulus must be thought of, while in women of like age gall- 
stones are common. At this time malignant disease is possible in either. 
Fecal impaction may be found at any period. Finally the exact nature 
and site of the lesion can often be determined only by operation. 

The Blood. — A leukocytosis is regularly present in acute obstruction. 
In some cases the count shows 50,000 or even 80,000 leukocytes to the 
cubic millimeter. 

Prognosis. — Acute intestinal obstruction is nearly always fatal un- 
less promptly relieved. Children will occasionally recover from intus- 
susception without operation, but the possibility is too slight to be of 
value. Obstruction from gall-stones or fecal impaction may also yield 
naturally, but the attacks will be repeated unless the cause is removed. 

Treatment. — In any case of suspected acute obstruction feeding 
should be stopped. Purgatives must not be given. The persistent 
vomiting may be relieved by repeated washing of the stomach. The 
bowel below the obstruction may be emptied by enemata of warm water, 
soap-suds or olive oil. In giving injections the amount of fluid retained 
should be carefully measured as an indication of the patency of the 
colon. In adults the capacity of the colon may amount to six quarts. 
For the relief of pain morphine may be given hypodermatically. For 
the distention turpentine stupes to the abdomen are indicated. Intus- 
susception in children may sometimes be relieved by the injection of 
water or air into the rectum and colon. For this purpose the child is 
anesthetized, placed upon an inclined plane Avith the head downward, 
and water is then aUowed to flow from a fountain syringe, suspended 
not more than three feet above the level of the table, into the colon. The 
passage of the water upward in the colon may be followed by observation 
of the abdomen, and the reduction of the intussusception may be favored 
by gentle manipulation of the tumor, if it can be felt. Instead of the 
water air may be injected from a Davidson's syringe. These measures 
are applicable only in the early stages of intussusception (the first 24 
hours) and are always attended with some risk of rupture of the weak- 
ened intestine. In the event of their failure or of the return of symp- 
toms after temporary disappearance, the abdomen should be promptly 
opened and the intussusception reduced by traction and manipulation. 
In all other cases of acute obstruction operation is imperative as soon 
as the diagnosis is made. In cases of chronic obstruction the diet should 
be restricted, the bowels moved by enemata, and operation undertaken 
as soon as the permanency of the ol)struction is established. 



DISEASES OF THE INTESTINES 



107 



CONSTIPATION 

Etiology. — Normal defecation is the result of the co-ordination of a 
number of factors. Feces accumulatino- in the rectum and colon excite 
the mucous membrane from which nerve impulses travel to a center in the 
lumbar cord and there cause motor impulses which result in increased 
peristalsis of the intestine and a simultaneous relaxation of the sphincter 
ani. The cerebrum exercises a certain degree of control over the lower 
centers in the cord and may thereby inhibit or augment their action. 
Furthermore, in the final operation the voluntary muscles of the abdomen 
as well as those of respiration are called into action, so that the process 
can be materially modified by conscious action. Constipation may result 
from interference with any of these several steps. 

1. Modification of the fecal contents by too scanty or otherwise 
unsuitable food, or by disturbances of digestion in the stomach or 
intestine. 

2. Impaired sensibility of the intestinal wall, as the result of disease 
or injury — such as occurs in certain forms of colitis, or atrophy of the 
mucous membrane. The taking of drugs, especially opium or its deriva- 
tives, probably operates in this way. 

3. Impairment of any part of the reflex nervous mechanism by 
which the sensory impulse is translated into motor discharges, such as 
occurs in many nervous diseases, particularly those affecting the cord. 

4. Inattention to or inhibition of the natural impulses to defecation. 
Infants over six months of age can be trained to have a defecation at a 
regular hour. In children particularly, but often in adults as well, the 
same influence of habit can be seen. Constipation may be said to be a 
normal condition in idiots and the insane. 

5. Lack of muscular power in the colon or in the voluntary muscles 
which take part in the process. Loss of power in the colon is seen in 
many cases of chronic inflammation of the colon, in hysteria and neuras- 
thenia. In conditions of relaxation of the abdominal muscles, such as 
follows pregnancy, constipation results. 

6. Lack of normal exercise affecting these muscles. Constipation is 
almost unkno^^Ti in workmen whose occupations call for abundant use 
of the abdominal and respiratory muscles. It is the rule in men of 
sedentary life. 

7. Abnormalities Avhich interfere with the emptying of the rectum 
and colon. In children the extreme length of the sigmoid operates in 
this way. Later in life strictures of all kinds are met with. Tumors 
of other parts, such as fibroids of the uterus, by pressure upon the intes- 
tine, may obstruct it. 

8. Spasm of the sphincter ani. This is not an infrequent form of 
obstruction. Spasm may be the result of excessive nervous irritability, 
such as is seen in neurasthenia, or it may result from the presence of 
local conditions, ulcers, fissures, or other painful affections of the anus. 



108 



DISEASES OF THE DIGESTIVE SYSTEM 



In most cases of constipation several of these factors are combined 
to bring about the result. 

While the conditions under which constipation is met with are 
manifold, the condition is most closely associated with the acute fevers, 
chronic diseases of the stomach, intestine or liver, and the various 
anemias, especially chlorosis. 

Constipation in infants may result from congenital abnormalities of 
structure or function. The long sigmoid flexure is a factor of impor- 
tance, and congenital strictures, as well as imperforate anus, are kno^vn. 
Most often constipation in infants is the result of improper feeding and 
lack of training. The habit so developed may last throughout life. Con- 
densed milk and various proprietary foods by reason of deficiency in 
fat may produce constipation. Anemia, rachitis, and other organic dis- 
eases are causes of importance. 

Symptoms. — Constipation for long periods may be borne without 
discomfort by some. It is, however, usually associated with headache, 
lassitude, loss of appetite, possibly nausea, and malaise. The tongue is 
coated and the breath offensive. Fever is also present at times. In 
young children constipation quite regularly gives rise to attacks of 
fever, fretfulness^ and vomiting. In extreme cases the feces form 
masses in the rectum or colon, which may obstruct the bowels, enor- 
mously distend the part in which they lodge and cause enteritis, or 
even perforation and peritonitis. A doughy tumor which can be in- 
dented by the finger is found either in the abdomen or by rectal examina- 
tion. Hemorrhoids or anal fissures may be caused by the pressure of 
fecal masses. 

Treatment. — In many cases this must be by the removal of the 
cause, such as the pressure of a tumor, the cure of an anal fissure, the 
removal of a mass of hardened feces, or the treatment of the associated 
neurasthenia, hysteria, or anemia, or disturbances of the other digestive 
organs. At the onset of acute fevers we relieve constipation by a full 
dose of calomel and salts, or castor oil, or a simple enema. During the 
course of such fevers the bowels had best be moved by enema. 

To treat the habit of constipation properly we must combine : ( 1 ) 
Regularity of habit, a fixed hour for defecation observed daily. (2) 
Exercise for the abdominal muscles, such as (a) Standing erect and 
bending to touch the fingers to the floor without bending the 
knees. (b) Lying flat upon the floor and raising the body 
by the pelvic muscles without using the hands. This exercise can be 
made more effective by hooking the toes under some support, as the 
end of a bed, and swinging forward against the knees as a rower does 
in rowing, (c) Hooking the thumbs together with arms extended above 
the head and then swinging as far as possible from side to side. Such 
exercises should be practiced for 10 to 15 minutes on rising. When 
exercises cannot be taken, massage to the abdomen nmy be substituted, 
or a cannon-ball weighing 4 to 6 pounds may be rolled over the abdomen. 
(3) Diet, suited to the individual di^'restion. Concenti-ated foods, leav- 



DISEASES OF THE INTESTINES 



109 



ing little residue, such as milk and eggs and meat, are undesirable. 
Oatmeal, graham breads, or brown bread, which leave much residue 
are helpful. Fruits of all kinds, but especially oranges, figs, dates and 
apples, are laxative in effect. A glass of water, hot or cold, sipped 
before breakfast, is of value. Coffee and tobacco help some persons. 
Drugs are to be used only in the failure of hygienic and dietetic meas- 
ures. Cascara sagrada is given, 5 to 10 grains of the extract in pill, 
each night or in smaller doses after each meal. Rhubarb and soda 
mixture, pills of aloin, belladonna and strychnine, or combinations of 
these drugs with podophyllin, are often used. Suppositories or enemata 
may be required. In that case, suppositories of glycerine, or enemata of 
warm water, soap-suds, or olive oil may be used. In the obstinate con- 
stipation of neurasthenia or hysteria, high injections of 1 to l^/o pints 
of warm olive oil may be the only remedy. Enemata of water or oil 
may be used for years in some cases without harm. 

In infants the measures of most value are (1) increase in the per- 
centage of fat as high as can be borne; (2) the use of oatmeal instead 
of barley water in the food; (3) the addition of orange juice. A conical 
piece of soap may be inserted into the anus and held there for a few 
minutes. Glycerine suppositories may be used. Abdominal massage 
is of value. If medicines must be used milk of magnesia is best, one or 
two teaspoonfuls added to the evening feeding. Rhubarb and soda or 
preparations of cascara sagrada may be used for a time. 

ENTEROPTOSIS 
(Glenard's Disease ) 

Definition. — An abnormal downward displacement of the intestines 
(usually also the other abdominal viscera). Thus we may see gastrop- 
tosis, splenoptosis, hepatoptosis, or nephroptosis. 

Etiology. — The condition may be congenital or may in later life 
be due to relaxation of the various abdominal ligaments produced by 
repeated pregnancies, ascites, or the like. In some cases increased 
weight of the individual viscera, such as occurs in dilatation of the 
stomach or enlargement of the spleen or kidney, is the cause. It also 
develops in certain patients without discoverable cause. 

Symptoms. — There may be none, or the displaced viscera, especially 
the spleen, liver, or kidney, may cause more or less constant dragging 
pain or discomfort. The latter symptoms are sometimes associated with 
symptoms of neurasthenia or hysteria, if the patients know of the vis- 
ceral displacement. Rarely the displaced viscus, spleen, or kidney may 
cause symptoms by pressure on other abdominal organs, such as the 
uterus, stomach, or appendix. Chronic obstruction of the intestine may 
result from kinks or twists. 

Treatment. — (1) Abdominal supports of various kinds have been 
designed to meet the indications. (2) The neurasthenia or hysteria 
must be treated, and the general health guarded. (8) Rarely operative 



110 



DISEASES OF THE DIGESTIVE SYSTEM 



replacement, or removal of a displaced viscus is called for. (See En- 
largement of Spleen and Floating Kidney.) 

The use of the X-raj^s following the ingestion of a gruel or paste 
containing an ounce of bismuth subcarbonate most accurately locates the 
position of the stomach, and if the course of the bismuth downward be 




Fig. 20. — Gastroptosis with dilatation of the stomach. Radiograph after administration of emulsion 

of bismuth. 

followed the position of the intestines. Obstruction may be revealed 
by delay in the onward passage of the bismuth. To determine the posi- 
tion of the colon, enemata of bismuth are employed. (See Figs. 20 
and 21.) 

NEUROSES OF THE INTESTINE 
(Nervous Diarrhea) 

Definition. — A functional motor disturbance of the intestine 
producing diarrhea. 

Etiology. — (1) The exciting cause is powerful emotion, such as 
grief, anger, or fear. The looseness of the bowels experienced by many 
speakers just before or after a public appearance is a good example. (2) 
The underlying cause may be malnutrition, anemia, or neurasthenia. 



DISEASES OF THE INTESTINES 



111 



The affection sometimes appears in association with nervous diseases, 
such as exophthalmic goitre or locomotor ataxia. 

Symptoms. — Frequent loose, watery movements of the bowels are 
characteristic. These may occur at any time of day or follow regularly 
the taking of food. The excessive peristalsis is often accompanied by 
audible rumbling or gurgling. The course of the affection may be very 




Fig. 21. — Ptosis of the transverse colon. An emulsion of bismuth subcarbonate has been injected 
per rectum and the patient required to lie for five minutes first upon the left side, then upon the back, 
then upon the right side. The loops of the colon at the hepatic and splenic plexuses are caused by the 
ptosis of the transverse colon. This condition is not uncommon and its pathologic importance is 
doubtful. 

brief, limited to the inunediate action of the exciting causes. In other 
instances the underlying conditions are the important ones and the 
condition persists with periods of improvement until they are relieved. 

Treatment. — Release from nervous excitement may be all that is 
required. In the protracted cases we must treat the underlying condi- 
tion rather than the diarrhea. To this end change of scene and air may 
contribute. In extreme case the rest cure may be required. Limitation 
of the diet to easily digestible foods is indicated. Opiates should not be 
given and astringents are of no value. Nerve tonics, such as asafetida, 
valerian, arsenic, or the glycerophosphates, are indicated. 



112 



DISEASES OF THE DIGESTWE SYSTEM 



MUCOUS COLITIS 
(Membranous Colitis ) 

Definition. — An affection characterized by attacks of abdominal pain 
or discomfort and the passage of masses of mncus often in the form of 
shreds or casts of the bowel. 

Etiology. — The disease belongs to the years between 30 and 50. bnt 
may develop in yonnger or older persons. Women, more often than 
men, are affected. Xenrasthenia, hysteria, or the nervous temperament 
is regularly associated. 

It is often secondary to chronic constipation or to chronic appen- 
dicitis or dysentery. 

Morbid Anatomy. — No definite lesions of the colon have been 
demonstrated. The bowel may be either dilated or contracted. 

The mucus discharged is usually in the form of large colorless or 
whitish gelatinous masses or shreds or casts of the bowel. It may simply 
coat the surface of a formed stool or be mixed with fecal material, or 
constitute the entire passage. 

Symptoms. — The onset of the disease is gradual and the process is 
usually well developed before it is recognized. Attacks of abdominal 
discomfort, soreness, or severe colic occur from time to time and accom- 
panying or foUo^^dng the attacks of pain, the patient passes stools con- 
sisting wholly or in great part of mucus. The mucus may appear in 
masses, or have the form of a cast of the bowel, the patient often being 
persuaded that the "lining of the bowel" has been passed. In the 
intervals between attacks the patient suffers from chronic constipation. 
Lack of appetite, nausea, heaviness or discomfort after eating, abdominal 
distention, gaseous eructations, heart-burn and the like s^miptoms of 
''nervous dyspepsia" may be complained of. The patients become thin 
and possibly anemic. Neurasthenia, melancholia, or hysteria is often 
present in marked degree. The affection is very chronic and may con- 
tinue indefinitely with periods of remission and exacerbation. 

Examination of the abdomen at the time of the attacks shows it 
either distended or flattened, often very tender to pressure, especially 
on the right side. On inspection of the bowel through a speculum, it 
may be found distended or contracted, its surface may appear congested, 
but usually shows only a coating of mucus. I'lcers or other organic 
lesions are rarely found. 

The patient sho^vs the general charactei'^ of hysteria, neurasthenia, 
or melancholia. 

Diagnosis. — The passage of masses, or casts of mucus associated with 
abdominal pains, digestive disturbances and general nervous manifesta- 
tions is usually diagnostic. The severe attacks often suggest acute 
appendicitis, but fever and leukocytosis are absent, and the recurrence 
of the attacks with the mucous stools diagnostic. Chronic appendicitis 
can be excluded only with great difficulty, except by the general dift'u- 
sion of the pains over the abdomen and the absence of focal signs. 



DISEASES OF THE INTESTINES 



113 



Other causes of abdominal pain, such as renal or ureteral stone, dis- 
ease of the tubes or ovaries, appendicitis and the like, must be excluded. 

Prognosis. — Mucous colitis is never fatal of itself, but tends to 
become chronic and incurable. Prompt and permanent cure may, how- 
ever, be effected. 

Treatment must be adapted to the patient. 

The relief of chronic constipation by dietetic and hygienic measures 
often cures mucous colitis. (Von Noorden.) The institution of a proper 
diet with exercise and the free use of water may be all that is required. 
Laxatives should be used only in case of necessity, but some patients are 
relieved by occasional doses of castor oil. Daily lavage of the colon 
with water containing the fluid extract of hamamelis (oj to the pint) 
or nitrate of silver or quinine 1/5000. This should be practiced for a 
short time only. Injections of olive or cotton seed oil (8-12 ounces) at 
bedtime are helpful to some. 

Abdominal massage or electricity may be used. Neurasthenia or 
hysteria must be appropriately treated. And finally surgical measures, 
such as the removal of a chronically inflamed appendix or an appen- 
dicostomy to allow free irrigation of the colon from above downward, 
may be necessary. 

CANCER OF THE INTESTINE 

Etiology. — Cancer of the intestine, including both large and small 
intestine, is comparatively common. About 50 per cent, of all cancers 
are found in the alimentary tract, 8 per cent, of all in the intestine. 
Most cases occur m the period between 40 and 60 years, a few earlier. 
Cancer of the rectum is more common in men. 

Morbid Anatomy. — Cancer of the intestine is nearly always pri- 
mary, rarely metastatic. The new growths are of various types. The 
most common is the cylindrical epithelial groAvth infiltrating the wall 
of the intestine; medullar}^ carcinoma, forming soft, sometimes cauli- 
flower-like tumors, readily ulcerating and producing hemorrhages, is 
not infrequent. Colloid and scirrhous growths are both rare and, if 
present, are usually in the rectum. 

Carcinomatous growths may develop in any part of the intestine, 
but are most common in the rectum. They form more or less extensive 
growths infiltrating the wall of the intestine, usually constricting it, show- 
ing on the internal surface ulceration of the character seen in cancer of 
the stomach, and producing by extension into surrounding parts a tumor 
of varying size. There may be extensive adhesions about the affected 
part of the gut, partly due to invasion, partly to secondary local perito- 
nitis. If perforation occurs a localized abscess or a general peritonitis 
is found. 

Symptoms. — Cancer of the intestine presents several different clin- 
ical pictures. 

1. Cases marked by intestinal obstruction. The constriction of the 
8 



114 



DISEASES OF THE DIGESTIVE SYSTEM 



intestine may produce obstruction before any other symptoms appear. 
The obstruction is naturally gradually progressive. The history is 
therefore of repeated attacks of more or less severe constipation, relieved 
in one or another manner, terminating in an attack of undoubted intes- 
tinal obstruction, with complete obstipation, nausea, fecal vomiting and 
abdominal pain. On examination the abdomen is found distended, 
slightly tender, tympanitic. A tumor may be palpable in the abdomen 
or may be felt per rectum, but in many cases neither the presence nor 
location of a growth can be made out. Peristaltic waves in the intestine 
may be observed, and study of these and the location of the abdominal 
distention (whether of the small intestine, or colon, or both) may sug- 
gest the location of the gro^i:h. 

2. Cases marked by obstruction and ulceration. These are most 
common in the rectum. Increasing constipation with small, possibly 
ribbon-like stools, with traces of blood, or muco-pus is the rule. In other 
cases frequent small passages, attended with straining and containing 
much pus and blood and little fecal matter, are reported. In either case 
examination of the rectum by the finger or the proctoscope locates a 
groAvth in the rectum, often in the lower part. Pain is usually not severe 
in the early stages. With ulceration it becomes more and more severe. 
Cachexia develops relatively late. Fever occurs only in advanced cases. 

3. Cases in which the cachexia and possibly fever are present for 
some time before the growth presents localizing symptoms. In rare 
cases old people suffering from cancer of the intestine present no evi- 
dences but cachexia and an irregular fever. 

Course. — Carcinoma of the intestine grows, gradually invading 
adjacent structures, producing metastases, especially in the liver, and in 
time causing death either from intestinal obstruction, or pain and 
cachexia, or such complications as abscess or cystitis caused by localized 
extension, or general peritonitis. The duration of life after diagnosis 
varies greatly. Cancers of the rectum are usually discovered early, 
those of the intestine or colon late. Cases with marked intestinal obstruc- 
tion are ordinarily promptly fatal. Removal may bring temporary re- 
lief. Life in any case is rarely prolonged beyond a year. A few cases 
of recovery from cancer of the rectum are kno^^Ti. 

Diagnosis. — In either acute or chronic intestinal obstruction in a 
patient beyond 40 years of age the possibility of a new growth of the 
intestine must be considered. Marked secondary anemia and cachexia 
strengthen the suspicion. A local tumor of the intestine almost estab- 
lishes the diagnosis. 

Such growths are usually freely movable, but mR-y be fixed by adhe- 
sions. They are firm, slightly tender, do not indent on pressure. Fecal 
impactions must be excluded, remembering that fecal tumors may form 
above the stricture of a new growth. Repeated enemata or colon irri- 
gation may be employed to aid diagnosis. In many cases the diagnosis 
can be made only after opening the abdomen, possibly only on micro- 
scopic examination of the growth. 



DISEASES OF THE LIVEE 



115 



Rectal carcinomata, being accessible either by the finger or procto- 
scope, can as a rule be easily recognized. They form dense cylindrical or 
polypoid growths infiltrating the wall of the intestine, stenosing it, 
showing ulceration on the surface, bleeding readily, and movable or 
fixed, depending upon involvement of adjacent structures. Syphilitic 
stricture must be excluded, by the history, by the absence of dense infil- 
tration or deep ulceration, failure of the Wassermann reaction, and 
the results of treatment. 

Tubercular ulceration implies tuberculosis elsewhere, less infiltration 
and the presence of tubercle bacilli in the mucus of the feces. 

If the growth is accessible microscopic examination of fragments 
taken from the edge of an ulcer may be employed. Rarely fragments 
of these growths can be found in the feces. 

The urine will show indican in abundance. The blood examination 
indicates severe secondary anemia. 

Treatment must be surgical or merely palliative. Removal of the 
growth, if feasible, should be tried. Exposure to the emanations of 
radium has been helpful in non-operative cases, especially those of the 
rectum. 

DISEASES OF THE LIVER 

JAUNDICE 

Definition. — Jaundice is the pigmentation of the skin, conjunctivae 
and other tissues or fluids of the body by bile-pigments. Formerly it 
was taught that jaundice might be produced either by obstruction to 
the bile-ducts with resulting reabsorption of bile-pigment into the blood 
or by excessive destruction of red-blood cells, the hemoglobin derived 
from which was converted into bile-pigment, and jaundice was there- 
fore classified as (1) obstructive or hepatogenous and (2) non-obstruc- 
tive or hematogenous. We now know that the latter condition is also 
due to obstruction to the flow of bile, produced by increased viscidity 
of the bile and possibly by a catarrhal swelling of the finer bile-ducts in 
the liver. The latter is therefore designated as toxemic jaundice, and 
for clinical convenience we restrict the term obstructive jaundice to the 
cases in which there is obstruction of the larger bile-ducts. 

OBSTRUCTIVE JAUNDICE 

Etiology. — This may be due to (1) inflammatory swelling of the 
mucous membrane of the duodenum and common duct; (2) obstruction 
of the common duct by gall-stones, parasites or other foreign bodies; 
(3) by pressure from without, especially by tumors of the head of the 
pancreas, the liver, kidney, stomach or omentum; (4) by tumors growing 
in the wall of the duct itself; (5) by stricture or obliteration of the 
duct. Obstruction of the cystic duct does not give rise to jaundice. 

Symptoms. — (1) Icterus or the pigmentation of the skin and con- 



116 



DISEASES OF THE DIGESTIVE SYSTEM 



junctiva. This varies from a faint j^ellow to a deep olive-green in the 
permanent obstruction. All the other tissues of the body may be more 
or less stained. (2) Absence of bile in the stools, giving rise to slate- 
gray or clay-colored stools. Constipation is regularly present and the 
stools are hard and dry. (3) Presence of bile in the urine and sweat. 
The color of the urine becomes darker, with a greenish-yellow tinge. In 
extreme cases it may be almost black. The sweat may be sufficiently 
tinged to discolor the linen. (4) Slow pulse: the pulse falls to 40, 30 
or even 20 per minute. Frequently the temperature is subnormal at the 
same time. These effects are attributed to the action of the bile-salts 
and disappear in chronic jaundice because in the end the liver loses its 
power to secrete these salts. These symptoms are therefore most char- 
acteristic of catarrhal jaundice. (5) Itching of the skin is a common 
and sometimes very annoying feature of jaundice. (6) Hemorrhagic 
tendency: in protracted jaundice the coagulation time of the blood 
may be ten to twelve minutes instead of the normal of three or four. 
Bleeding may occur from the mucous membranes or into the skin. This 
tendency to bleed magnifies greatly the danger of operations upon these 
patients. (7) Cerebral symptoms: headache, lethargy, and melancholia, 
are characteristic of the early stages of jaundice. In the later stages and 
in the severer forms, delirium, coma and convulsions may develop. 
Frequently with these symptoms the patients have an increasing fever, 
dry tongue, a rapid pulse and all the other symptoms of a severe intoxi- 
cation. This condition is spoken of as cholemia, as though produced by 
the bile-salts, but at present there is no good evidence that such is the 
case. 

TOXEMIC JAUNDICE 

This occurs in a variety of conditions: (1) As a result of poisons, 
such as phosphorus, arsenic or snake-venom. Experimentally it is read- 
ily produced by toluylencliamin. (2) Various specific infections, 
malaria, pyemia, relapsing, scarlet, typhoid, typhus, or yellow fever. 
(3) Various obscure conditions, such as acute yellow atrophy, Weil's 
disease, icterus gravis, etc. 

Apart from a slight tinting of the skin and conjunctiva, these eases 
usually show no symptoms directly referable to the jaundice. The urine 
shows little or no bile, while the feces have their normal color. In the 
severer forms the color may be more marked and in some cases there 
are high fever, delirium, coma or convulsions, black vomit and hemor- 
rhages into the skin. 

ACUTE YELLOW ATROPHY OF THE LIVER 

Definition. — A rare, acute disease, characterized by widespread 
necrosis of the liver cells and by jaundice with severe toxic symptoms. 
Etiology. — 1. It occurs without discoverable cause. 
2. It occurs secondarily to pregnancy or to various acxite infections, 



DISEASES OF THE LIVER 



117 



such as syphilis, pyogenic infections, typhoid or malarial fever, or diph- 
theria. About one-half the cases occur in women during pregnancy. It 
occasionally occurs in childhood. 

Chloroform and phosphorus-poisoning present similar necrosis of 
liver cells. The designation, acute yellow atrophy, has been used to 
cover a group of disorders whose chief point of agreement lies in the 
acute necrosis of the liver. 

Morbid Anatomy. — The liver is one-half to one-third normal size, 
flaccid, the capsule wrinkled. The color is changed to a greenish-yellow 
or dirty gray-brown. Subserous hemorrhages may be present. The 
liver cuts with resistance, the section shows the same color as the sur- 
face; hemorrhages may be present. ]\Iicroscopically there is a general 
necrosis of the liver cells, with hemorrhages, and round-celled infiltration 
of the interstitial tissue. The section may hardly be recognizable as 
liver. The changes in the other organs are not constant. The tissues 
are usually jaundiced and sometimes show hemorrhages. 

Pathogenesis. — The process is now regarded as an autolysis of the 
liver brought about by the destruction of the liver cells by some unknown 
poisons, the liver cells being then digested by proteolytic ferments which 
they normally contain. 

Symptoms. — (1) An initial stage, lasting from a few days to a week, 
of malaise, poor appetite, coated tongue, constipation and occasional 
vomiting. Slight jaundice is usually present in this stage. (2) Symp- 
toms of intense toxemic jaundice. The jaundice deepens, the vomiting 
becomes frequent, diarrhea may develop, hemorrhages occur from mu- 
cous membranes or into the skin, the patient becomes delirious or 
comatose, or has frequent convulsions, fails rapidly and dies in coma. 
A moderate fever may be present in the early stages. At the end the 
temperature is subnormal and may be so throughout. During this stage 
the liver dulness diminishes rapidly and may at the end be absent. The 
urine is reduced in amount and contains, besides albumin and casts, 
leucin and tyrosin and various organic acids. The amount of urea is 
reduced, the ammonia relatively increased. The blood shows a leuko- 
cytosis and from concentration an increase in red cells. 

Diagnosis. — In the first stage this cannot be made. Later the com- 
bination of jaundice, severe toxemia, reduction in the size of the liver, 
and the urinary changes is unmistakable. 

Prognosis. — The disease is regularly fatal in from five days to two 
weeks. A few recoveries have been recorded. 

Treatment. — In pregnant women the occurrence of severe toxemia 
or jaundice should excite suspicion. Careful examination of the urine 
(nitrogen partition) may then show a grave disturbance of metabolism. 
Appropriate treatment may avert the development of acute yellow 
atrophy. These patients must be kept in bed, on a fluid diet, preferably 
milk, with as much water as possible. The bowels must be kept open. 
Colon irrigations with warm normal salt solution are useful by increas- 
ing the flow of urine and })ossibly directly increasing elimination. The 



118 



DISEASES OF THE DIGESTIVE SYSTEM 



treatment of the fully developed condition must be directed to the acid 
intoxication present. The diet should consist of milk and cereals. The 
bowels should be kept freely open. Water is given freely. Enteroclysis 
or hypodermoclysis may be employed. Otherwise the treatment must be 
symptomatic. 

Icterus Neonatorum. — New-born infants may suffer from jaundice. 
(1) Physiological, so-called. In this form the jaundice develops on the 
second or third day of life and persists for one or two weeks. Thirty 
to sixty i^er cent, of new-born children have it. There are no symptoms 
other than the pigmentation and no treatment is required. The jaundice 
is undoubtedly due to bile, as bile-salts may be found in the urine, but 
the explanation of its occurrence has not yet been given. (2) Per- 
sistent jaundice, due either to (a) obliteration of the bile-ducts, (b) 
syphilitic hepatitis, (c) sepsis, especially that caused by umbilicaL in- 
fection. In the latter form the infants have high fever, rapid pulse, 
and other evidences of sepsis. Jaundice from these causes persists, the 
infant gradually loses strength and regularly succumbs. Treatment is 
of no avail. 

DISTURBANCES OF THE HEPATIC CIRCULATION 

1. Anemia of the liver is seen post-mortem in fatty or amyloid 
organs, or after hemorrhage. It produces no clinical symptoms. 

2. Hyperemia is common to many diseases: 

a. Acute Congestion. — An active hyperemia of the liver regularly 
follows a full meal, especially if accompanied by alcohol. Acute con- 
gestion seems also to be produced by the toxins of certain infections, 
such as malaria, yellow, typhus and typhoid fevers, erysipelas. The 
liver dulness may be slightly increased and the edge may be palpable, 
but there are no definite symptoms. 

Treatment. — A calomel or saline purge may be given. Otherwise 
the underlying condition is to be treated. 

b. Passive Congestion. Chronic Congestion. Nutmeg Liver. — This 
results from obstruction to the return of blood from the liver due to: 
(1) Failing compensation of the heart, resulting from disease of the 
valve or muscle, especially when the right side is involved. (2) Obstruc- 
tion of the pulmonary circulation, such as occurs in emphysema, inter- 
stitial pneumonia, large pleuritic effusions or intrathoracic tumors. 

Morbid Anatomy. — rThe liver is enlarged, firm, dark, and bleeds 
freely on section. The cut surface shows the characteristic nutmeg ap- 
pearance, from dilatation of the central veins of the lobules, pigmenta- 
tion of the adjacent cells, and fatty infiltration of those on the periphery. 
In long-standing cases there may be more or less cirrhosis, both between 
and within the lobules. 

Symptoms. — (1) Fulness or pain in the right hypochondrium. (2) 
Gastro-intestinal catarrh and hematemesis may result from accompany- 
ing congestion of stomach and intestines. (3) Slight jaundice may de- 
velop with bile in the urine and clay-colored stools. ' 



DISEASES OF THE LIVER 



119 



Physical Signs. — The liver is enlarged and may be palpable some 
distance below the costal margin. It may be tender, and in some cases 
pulsates. The pulsation so caused must be carefully distinguished from 
that communicated from the heart or aorta. 

Treatment. — (1) Free purgative salts may relieve the hepatic con- 
gestion. (2) Blood has been aspirated directly from the liver, but this 
practice is rarely followed. (3) Ilematemesis or spontaneous bleeding 
from piles sometimes accomplishes the desired result. 

DISEASES OF THE BLOOD-VESSELS OF THE LIVER 

HEMORRHAGE 

Bleeding into the substance of the liver may result from (1) trauma, 
(2) acute yellow atrophy or phosphorus-poisoning, or (3) such diseases 
as purpura, scurvy, leukemia, malaria, abscess or cancer. The hemor- 
rhages may be single or multiple. In rupture the blood may be poured 
into the peritoneal cavity and syncope or death result. 

EMBOLISM OR THROMBOSIS 

(1) Emboli originating in any part of the portal territory may lodge 
in the liver. Infarction is rarely produced owing to the free anas- 
tomoses of the hepatic artery. If the emboli are septic, a suppurative 
pylephlebitis may result. (2) Thrombosis may occur in (1) cirrhosis, 
(2) cancer, (3) sclerosis with roughening of the vessel wall, as in Banti's 
disease, (4) local inflammation from trauma, abscess, or foreign bodies. 

Morbid Anatomy. — The condition is that of a more or less complete 
portal obstruction. The collateral circulation may be well developed. 
The portal vein may be reduced to a fibrous cord. 

Symptoms. — The obstruction, if sufficient, produces the same symp- 
toms as cirrhosis. 

Treatment. — The treatment is also that of cirrhosis. 

SUPPURATIVE PYLEPHLEBITIS 

Etiology. — Suppurative inflammation of the portal vein results from 
the lodgment in the vein of septic emboli derived from any part of the 
portal territory, as from gastric or intestinal ulcers, from appendical 
or pelvic suppurations. Infection of the umbilicus in the new-born may 
have this result. 

Symptoms. — (1) In some eases multiple abscesses in the liver are 
produced. (See Abscess of the Liver.) (2) In other cases the symp- 
toms are those of pyeixiia, with an enlarged, tender, and painful liver. 
The disease lasts for from one to four weeks and is invariably fatal. 

Affections of the hepatic artery and vein, such as dilatation, aneurism, 
embolism, or thrombosis, are met with post-mortem, but are not recog- 
nizable during life. 



120 



DISEASES OF THE DIGESTIVE SYSTEM 



CIRRHOSES OF THE LIVER 
PORTAL CIRRHOSIS (LAENNEC'S) 
(Chronic Hepatitis. Hobnail Liver. Alcoholic Cirrhosis. Atrophic Cirrhosis) 

Definition. — A chronic interstitial inflammation of the liver, result- 
ing in a great increase of the connective tissue, more or less atrophy of 
the parenchyma, with resulting obstruction to the portal circulation. 

Etiology. — This affection is most often seen in men over 40 years, 
but occurs in women of like age, and is not unknown in childhood. The 
causes are various: (1) Alcohol is the common one, especially the per- 
sistent use of distilled liquors, but wines or beer may act similarly. (2) 
Acute infectious diseases, such as scarlet fever, typhoid fever, and the 
like. (3) Tuberculosis and syphilis are occasionally complicated by 
cirrhosis of the liver. (4) Obstruction of the bile-ducts (chronic jaun- 
dice). (5) Toxins produced in the intestine in certain forms of dys- 
pepsia, such as lactic, acetic, or butyric acids, and the like. Such toxins 
are assumed to account for the cirrhosis of the liver found in splenic 
anemia and Banti 's disease in association with enlargement of the 
spleen. At least nine-tenths of all cases of cirrhosis of this type are 
caused by alcohol, which acts either (1) as a direct poison upon the 
liver cells, causing their degeneration with secondary fibrosis, or (2) 
by causing gastric and intestinal catarrh which result in the production 
of poisons having a like effect. 

Morbid Anatomy. — There are two typical forms, in both of which 
the essential feature is a marked increase in the interlobular connective 
tissue. ( 1 ) Atrophic cirrhosis : The liver varies greatly in size, some- 
times being reduced to one-half the normal, in other cases it is larger 
than normal. The weight may be similarly reduced, but in- the majority 
of cases exceeds the normal. The surface is rendered rough by con- 
traction of the fibrous tissue, between the bands of which the lobules 
form prominences, giving the hobnail appearance. The consistency is 
increased so that the organ feels hard and cuts Avith resistance. The 
section shows plainly the thickened strands of grayish connective tissue, 
between which lie the contracted lobules of liver cells. The color of 
the liver, both surface and section, is usually a taAMiy yellow (whence 
the name). Microscopically the thickened bands of connective tissue 
are prominent. Within them lie the branches of the portal vein, com- 
pressed, thrombosed, or even obliterated. The connective tissue is often 
densely infiltrated with small round cells. The biliary canaliculi fre- 
quently appear greatly increased in numbers. In many cases the growth 
of new connective tissue is not only interlobular, but intralobular as 
well. The changes in the liver cells vary greatly, many of them showing 
degeneration, others hyperplasia and regenerative processes. The reduc- 
tion in the size of the viscus is doubtless due to the disappearance of 
many cells. (2) Fatty cirrhosis: In this form the organ is enlarged. 



DISEASES OF THE LIVEE 



121 



its weight increased, even to ten pounds or more, smooth of surface, 
more yellow in color. It cuts with less resistance. On section the in- 
creased connective-tissue strands appear as in the atrophic form. On 
microscopic section a widespread fatty infiltration and degeneration of 
the liver cells is found. In other features it corresponds with the atrophic 
form. 

Associated Lesions. — The peritoneum is thickened and opaque. The 
spleen is regularly enlarged and hard, showing the changes of chronic 
congestion. The stomach and intestines are congested throughout, and 
especially near the esophagus and in the lower rectum greatly dilated 
veins are found. The kidneys often present the changes of chronic 
nephritis. Frequently a general arteriosclerosis and corresponding 
changes in the heart are present. These modifications of the heart, 
arteries, and kidney are dependent upon the underlying cause of the 
cirrhosis (alcohol) rather than upon the cirrhosis itself. 

Compensatory Circulation. — The portal circulation being ob- 
structed by the cirrhotic process in the liver, the blood seeks new chan- 
nels of return. These are regularly found in the enlargement of normal 
anastomoses or possibly by the formation of new vessels. (1) Anas- 
tomoses of the gastric and esophageal veins. (2) The veins of Retzius 
which unite the terminal branches of the intestinal and mesenteric veins 
with the inferior cava. (3) Anastomoses between the inferior mesenteric 
and hemorrhoidal veins, branches of the internal iliac. (4) Numerous 
veins which lie in the suspensory and falciform ligaments and connect 
the portal system with the mammary and epigastric veins, the accessory 
portal system of Sappey. Occasionally a large vein, the para-umbilical 
vein of Sappey, passes along the falciform ligament to unite at the 
umbilicus with branches of the epigastric veins. Enlargement of these 
veins about the umbilicus, in rare cases, produces the so-called caput 
medusae. (See Fig. 22.) 

Symptoms. — These are for the most part due to the portal obstruc- 
tion. The chronic congestion of the stomach, intestines, spleen, and 
peritoneum induces appropriate changes of function in each. There is 
a chronic catarrh of the stomach and intestines which expresses itself 
as a dyspepsia, sometimes with vomiting and constipation or rarely 
diarrhea. Such symptoms in an habitual user of alcohol, if accom- 
panied by enlargement of the liver, should always suggest the develop- 
ment of cirrhosis. We cannot, however, venture the diagnosis until 
more conclusive symptoms of portal obstruction appear. (1) 
Hematemesis occui:s at some time in a large proportion of these patients. 
It may be the first symptom of the condition. Hemorrhage is caused by 
rupture of some of the dilated veins of the stomach, especially those 
about the cardiac orifice, and may be profuse. The bleeding may be 
repeated. (2) Ascites: Sooner or later in all cases giving symptoms 
free fluid accumulates in the abdomen. The enlargement of the abdomen 
is frequently the first complaint. Once begun the effusion usually accu- 
mulates rapidly, and if remov(Hl returns within a few weeks. Large 



122 DISEASES OF THE DIGESTIVE SYSTEM 



accumulations give rise to great distress from weight and pressure upon 
the adjacent viscera, especially the heart and lungs. (3) Hemorrhoids 
are frequently caused by dilatation of the anal veins, and free bleeding 
may occur from them. Hemorrhage either from the stomach or rectum 
may temporarily relieve the patient. (4) The facies regularly assumes 
a characteristic appearance, the skin and conjunctiva pale, with a slight 
icteric tint in the latter, the lids relaxed and puffy, the nose enlarged, 
red, and covered with dilated veins. Excepting the touch of jaundice 
these features belong to any chronic alcoholic patient. The jaundice is 
explained by slight obstruction to the flow of bile through the inter- 
lobular bile-ducts. (5) Edema of the lower extremities may appear 
early, either from an associated nephritis or from the pressure of a 
large quantity of ascitic fluid upon the internal iliac veins and the 
vena cava. (6) Physical examination shows emaciation with an en- 
larged abdomen giving characteristic dulness and fluctuation. (See 
Ascites.) After the removal of the fluid the liver can be felt, its edge 
hard, its surface rough and granular (hobnail). The spleen also may 
be palpable. The veins of the abdomen are dilated, but the classic 
caput medusa is rarely seen. Hemorrhoids can usually be found. Edema 
of the feet and legs and the characteristic facies may be present, but 
are not essential. (7) The urine is scanty, of high specific gravity, and 
usually contains a trace of albumin and casts. The urea is diminished 
on account of the lessened activity of the liver. (8) Fever is usually 
absent, but a moderate temperature, 100°-101° F., may occur at times. 
(9) Cholemia: Not infrequently the end is marked by increasing mental 
dulness, stupor, coma, or convulsions, with or without an increase in 
jaundice, and with a rising temperature. Whether these symptoms are 
caused by final failure of the function of the liver or by uremia due to 
nephritis is not at present known. It is evident that just in proportion 
as the compensatory circulation is established in cirrhosis, the food 
escapes the detoxicating influence regularly exerted upon it by the 
liver. 

Course. — Usually the gastric symptoms are the earliest, but any of 
the above symptoms may be the first. If the cirrhosis be marked, ascites 
regularly appears within a few weeks or months. Once ascites begins 
it regularly recurs, after" steadily shortening intervals, until the patient 
succumbs to exhaustion or the so-called cholemia. Some few recover, the 
compensatory circulation developing sufficiently to relieve the portal 
engorgement. The duration of life after the onset of ascites is usually 
not more than 18 months to two years. 

Diagnosis. — This cannot be made with certainty until the appearance 
of ascites. The other causes of ascites must then be considered, especially 
carcinoma of the liver and tubercular peritonitis. Cancer of the liver 
is usually secondary, gives rise to greater enlargement of the liver, with 
irregular tumors. Pain is complained of. Cachexia is marked, and 
secondary deposits may occur elsewhere. Tubercular peritonitis is regu- 
larly associated with fever, the ascitic fluid is encysted, not free, there 



124 



DISEASES OF THE DIGESTIVE SYSTEM 



are masses or thickenings to be made out in the peritoneum, and the 
other signs of portal engorgement are lacking. Tuberculosis may be 
present elsewhere. Finally the examination of the ascitic fluid of cir- 
rhosis shows a specific gravity below 1015, from 1 to 3 per cent, of 
albumin, and microscopically chiefly endothelial cells with a few leuko- 
cytes or blood cells. (See Tubercular Peritonitis.) 

Prognosis. — Cirrhosis of the liver is u.sually fatal in from two to 
three years from the onset of symptoms, or from one to two years after 
the development of serious symptom.s, such as ascites or hematemesis. 

Treatment. — All irritants must be stopped, especially alcohol. With 
severe gastric symptoms a milk diet may be required. Later the diet 
should be solid rather than fluid and of easily digestible foods. Nitrog- 
enous foods should be restricted. Constipation must be relieved, prefer- 
ably by hydragogue cathartics such as the heavy mineral waters or salts, 
compound jalap powder, or elaterine. Ascites, if slight, may be met by 
such catharsis and restriction of fluids. Sweating may be employed in 
strong patients. Tapping is regularly required and must be repeated 
according to the needs of the patient. A trocar and canula are used. 
The patient is seated. Strict asepsis must be practiced. Care must be 
taken to see that the bladder is empty. Then the trocar is intro- 
duced in the mid-line midway between the umbilicus and symphysis. 
As much as 20 quarts may be withdrawn. To avoid any possible danger 
from the sudden release of pressure, a many-tailed bandage should be 
applied to the abdomen from above downward, and pressure maintained 
as the fluid is withdrawn. Talma's operation for drainage and the 
furtherance of anastomoses has been successful in a number of cases 
and may be tried in vigorous patients. Otherwise treatment is purely 
symptomatic. 

BILIARY CIRRHOSIS 
(Hanoi's Cirrhosis) 

Definition. — A chronic, probably infectious, disorder of the liver, 
marked by cirrhosis, enlargement of the spleen and chronic jaundice, 
without symptoms of portal obstruction. 

Etiology. — The disease is frequent in India and rare in the United 
States. Alcohol probably bears no relation to it. Children of both sexes 
are frequently affected, while most of the adult cases occur in men. 
French writers who have devoted most study to the disease believe it 
infectious, but the active agent is unknown. 

Morbid Anatomy. — The liver is very large, weighing from 4.5 to 
9 lbs. (2000 to 4000 gms.), its surface smooth and dark olive green in 
color. The section is firm and of the same color. The connective tissue 
may be seen in bands outlining the lobes or extending into them. 

Microscopically the connective tissue is seen, and the invasion of 
the lobule is usually marked. In the brtuds of fibrous tissue are many 
bile eanaliculi showing catarrhal infiammation of their walls. The 



DISEASES OF THE LIVER 



125 



number of canaliculi is apparently much above normal. The liver cells 
show little or no degeneration. The invasion of the lobule by the fibrous 
tissue and the many fine bile-ducts showing inflammatory changes dis- 
tinguish the affection from portal cirrhosis. 

The spleen is greatly enlarged, weighing 1.3 to 2.6 lbs. (600 to 1200 
gms.), and shows fibrosis. All the organs are bile-stained. 

Symptoms. — The disease begins in childhood with digestive dis- 
turbances or without definite symptoms. (1) Gradually the patient 
becomes jaundiced and remains so, with all the symptoms of obstructive 
jaundice, except that the feces are dark and contain bile-pigments. (2) 
Attacks of pain in the right hypochondrium with fever, leukocytosis, and 
increase of the jaundice occur from time to time, and continue for days 
or weeks. (3) The spleen becomes enlarged and firm. Physical examina- 
tion shows deep jaundice, a large, smooth, sharp-edged liver and spleen, 
sometimes an enlargement of the tips of the fingers. The blood presents 
the picture of a secondary anemia with some leukocytosis. The urine 
shows the presence of bile. 

Course. — The disease is slowly progressive, usually lasting from 4 
to 5 or 10 years. The patients are likely to die with the symptoms of 
grave jaundice, high fever, delirium, coma, or convulsions, and hemor- 
rhages. 

Diagnosis. — From portal cirrhosis the disease is distinguished by 
its occurrence in the young and non-alcoholic, the marked jaundice, 
absence of ascites and other signs of portal obstruction, and chronic 
course. The attacks of fever with deepening jaundice and leukocytosis 
are important. Some cases can with difficulty be distinguished from 
Banti's disease. 

Treatment. — The use of antiseptics eliminated in the bile, such as 
urotropin or the salicylates, is advised. Otherwise the treatment must 
be symptomatic. 

ABSCESS OF THE LIVER 

Etiology. — 1. The solitary or tropical abscess. (1) Idiopathic cases 
are not infrequent in this country. (2) Dysentery is the common ante- 
cedent. Amebae, or staphylococci or streptococci may be found in the 
abscess. 

2. Embolic abscesses are common. These arise (1) from infective 
processes in the territory of the portal vein, such as appendicitis, typhoid 
fever, dysentery, etc.; (2) from systemic infections, such as ulcerative 
endocarditis, or pyemia. 

3. Trauma either to the body or head may cause a liver abscess. 

4. Suppurative cholangitis from any cause may cause multiple 
abscesses. 

5. Foreign bodies, such as needles or fish-bones, or parasites, 
such as round worms or echinococci, sometimes cause abscesses of the 
liver. 



126 DISEASES OF THE DIGESTIVE SYSTEM 



Morbid Anatomy. — 1. The solitary or tropical abscess is usually 
a single large abscess, either on the surface or in the substance of the 
right lobe. If the abscess be on or near the surface there is more or less 
perihepatitis. The abscess cavity is large and filled with pus mixed with 
blood and broken-down liver tissue, giving it a reddish-brown tinge like 
anchovy sauce or chocolate. The walls of the abscess are ragged and 
necrotic. Amebie may be found in the pus. Cultures may be sterile, or 
may yield bacillus coli, staphylococci or streptococci or other organisms. 
These abscesses may rupture into any of the adjacent viscera, the lung, 
pleura or peritoneum. 

In the single traumatic or idiopathic abscesses observed in New 
York the ameba is not found, but the common pyogenic organisms are 
obtained in cultures. Multiple abscesses : These are usually small and 
scattered throughout the liver, which is much enlarged. The surface is 
smooth. These multiple abscesses may center about the branches of the 
portal vein, the gall-ducts, the hepatic vein or artery. When the gall- 
ducts are involved the contents of the abscess are bile-stained, and gall- 
stones may be found. Suppurating echinococcus cysts are recognized 
by their contents. 

Symptoms. — 1. The Solitary Abscess. — There are regularly local 
and constitutional symptoms. (1) Local: (a) Pain, usually dull and 
aching, is complained of in the liver region. It may be referred to the 
back and right shoulder. Frequently the patient complains of a drag- 
ging sensation in the right side, when he lies upon the left, (b) The 
liver enlarges and becomes palpable. The increase in size is usually 
upward and to the right, so that the liver dulness rises abnormally high 
behind, even to the angle of the scapula, (c) The liver edge is tender 
to pressure, (d) In rare instances the abscess is so placed superficially 
that fluctuation can be detected or it may even rupture through the skin, 
(e) Other local signs may be produced by pressure upon adjacent organs, 
such as the lungs, whose embarrassment may give rise to dyspnea and 
cough. (2) Constitutional: These are those of sepsis, a fever of variable 
type, usually remittent, with more or less rapidity of the pulse, pros- 
tration and an increasing anemia. Loss of appetite, nausea or vomiting 
occurs at times, and there may be either constipation or diarrhea. Weight 
is ordinarily lost rapidly. The severity of both local and general symp- 
toms varies greatly so that these abscesses are sometimes classified as 
acute or chronic. The duration varies from one to two months to years. 
Perforation of the abscess into the lung occurs frequently, and after 
such relief recovery may occur. The pus discharged has a characteristic 
appearance and the ameb^e may be found in it. Rupture into other 
viscera, the stomach, intestine or pericardium, may occur with corre- 
sponding symptoms. 

II. Pyemic Abscesses. — The liver is enlarged, a little tender, and 
the conjunctivae present a slight icteric tint, but unless these symptoms 
are marked the condition is overlooked, by reason of the severity of the 
constitutional symptoms, which are those of pyemia. 



DISEASES OF THE LIVER 



127 



Prognosis. — This is always grave. The mortality is 50 per cent. 
Many patients succumb even after the abscess has been opened and 
treated with the greatest surgical skill. 

Diagnosis. — From malaria the septic fever ought easily to be dis- 
tinguished by the examination of the blood and the use of quinine. 

From empyema or abscess of the lung, or subphrenic abscess, the 
diagnosis is very difficult, if there is no history of dysentery or other 
cause to direct the attention to the liver. Here the line of dulness may 
suggest the presence of an abscess in the liver rather than fluid in the 
pleura. The liver may be palpable and very tender, and finally the pus 
obtained on aspiration may have the characteristics of liver pus and may 
even contain ameb©. 

From intermittent fever associated with gall-stones (intermittent 
hepatic fever of Charcot) the diagnosis may be made by (l).the 
long history of the latter, lasting years; (2) the fever, sweating, etc., 
occur in paroxysms separated by periods of complete freedom from 
fever; (3) the jaundice deepens after the paroxysms; (4) the general 
nutrition is maintained. 

The Blood. — Leukocytosis may be absent in amebic cases; in septic 
cases it is usually high, and the differential count gives an increased 
percentage of the polymorphonuclear cells. 

Aspiration of the liver may be employed. The needle may be inserted 
either in the axilla or behind in the middle of the dull area. A large 
needle must be used and introduced deeply. An anesthetic may be 
necessary. 

Treatment. — The large solitary abscess must be opened and drained. 
The small multiple abscesses cannot be treated. If an abscess is dis- 
charging through the lung, operation should be delayed, as many 
patients have recovered under these conditions. 

NEW GROWTHS OF THE LIVER 

The new growths of clinical importance are carcinoma and sarcoma. 
Angiomata, adenomata, and other forms of tumor are seen rarely even 
post-mortem and are not clinically recognizable. Echinococcus cysts, 
one form of tumor of the liver, are described elsewhere. 

Cancer of the Liver. — This is by all means the most frequent form 
of tumor. Cancer of the liver is primary in less than 5 per cent, of 
cases. The original focus is most frequently in the stomach, but may 
be in the gall-bladder, pancreas, rectum or other organs. Cancer de- 
velops in persons over 40 years of age, either men or women, and from 
causes at present unkno\^^l. 

Morbid Anatomy. — Three forms of primary cancer of the liver are 
recognized: (1) Nodular, 65 per cent, of all. The cancer occurs in the 
form of grayish-white, opaque nodules of varying size, scattered throngh- 
out the organ. Frequently the nodules are umbilicated. (2) ]\Iassive, 
23 per cent, of all. In this form there is one large tumor replacing to 



128 



DISEASES OF THE DIGESTIVE SYSTEM 



a great extent a whole lobe. (3) Infiltrating, 12 per cent, of all. In 
these cases the appearance is that of a diffuse cirrhosis (portal cirrhosis) 
of the organ, but on microscopic examination the connective tissue is 
found to be everywhere infiltrated with cancer cells. Secondary cancer 
of the liver regularly takes the nodular form described above. 

Symptoms. — These may at the outset be due to the primary growth, 
although in many cases such symptoms are lacking. Regularly a period 
of failing health, marked by languor, anemia, and possibly emaciation, 
precedes the development of symptoms which make the diagnosis pos- 
sible. (1) Tumor of the liver: The organ increases greatly in size, the 
edge and palpable surface are irregular (nodular). The enlargement 
is progressive and the liver is tender to pressure. In the massive type 
a definite tumor may be outlined. In the infiltrating type the liver feels 
exactly like the cirrhotic. (2) Jaundice regularly develops either from 
pressure upon the biliary passages outside the liver or from involvement 
of large numbers of them within the organ. (3) Ascites also develops, 
due either to pressure upon the portal vein or to involvement of the 
peritoneum, or in the terminal stages to the cachexia. In addition to 
these signs we have the symptoms characteristic of cancer in any loca- 
tion. Pain is usually present and is referred to the enlarged liver. 
Emaciation becomes marked and the cachexia extreme. Fever is absent 
or slight till the terminal stages: it may then be high. Edema of the 
feet and legs occurs toward the end, produced either by pressure upon 
the vena cava or by the anemia and cardiac weakness. In the infiltrating 
type the symptoms are those of portal cirrhosis, but with more rapid 
anemia and emaciation. The liver is enlarged, its surface rough, exactly 
as in cirrhosis. The diagnosis is rarely made during life. 

The hlood regularly shows an extreme secondary anemia. The red 
cells may number 2,500,000 or less. The leukocytes may be normal in 
number or increased, even to 25,000. 

Diagnosis. — The constitutional symptoms with the local signs of can- 
cer, when the latter develop, usually enable the diagnosis to be made. 
Other forms of enlargement of the liver, such as fatty or amyloid liver, 
cirrhosis, either portal or biliary, syphilis of the liver, or eehinococeus 
cyst must be excluded by careful study. Having made the diagnosis 
of cancer of the liver, we should in every case seek to locate the primary 
growth. For this purpose careful investigation of the abdominal viscera 
should be made. 

Prognosis. — The duration of life is given as from four to seven • 
months. 

Treatment. — Treatment is purely palliative. 

Sarcoma of the liver is exceedingly rare. Primary sarcoma is 
almost unknown. Secondarily the disease follows primary tumors of 
the skin, the bones, or the eye. It is to be remembered that primary 
melano sarcoma of the eye is peculiarly likely to be followed by 
metastasis in the liver. Clinically the disease is in all respects like 
cancer. 



DISEASES OF THE LIVER 



129 



FATTY LIVER 

Excessive deposition of fat in the liver may be due either to fatty 
infiltration or fatty degeneration of the liver cells. In this relation the 
distinction is not important. 

Etiology. — The important causes of fatty liver are (1) obesity, the 
liver being one of the storehouses of fat; (2) alcoholism; (3) cachectic 
states, as in the terminal stages of tuberculosis, the severe anemias, 
cancer, etc.; (4) certain gastro-intestinal disorders, such as occur in 
children. More or less deposition of fat occurs in the liver under the 
influence of many other poisons, especially the metallic poisons, arsenic, 
phosphorus, and the like, but not in sufficient amount to be of practical 
importance. 

Morbid Anatomy. — The liver is enlarged and may weigh 4 or 5 
pounds (4000 grammes), the surface pale and smooth, the section yellow 
and greasy, the consistency diminished. Microscopically the liver cells, 
especially in the periphery of the lobules, are infiltrated with fat ; in some 
cases the fat droplets apparently replace entirely the liver cells. 

Symptoms. — There are none directly attributable to the condition 
of the liver. On examination the liver is found enlarged, sometimes 
several centimeters below the costal margin. It is perfectly smooth, not 
tender or painful. 

Diagnosis. — This is based on the recognition of a painless, smooth 
enlargement of the liver, following the action of some appropriate cause 
and producing no symptoms. In childhood enlargement of the liver 
is regularly of this nature. 

Treatment. — Treatment is required only for the underlying 
condition. 

AMYLOID LIVER 

Amyloid degeneration of the liver is regularly part of such degen- 
eration, involving other viscera, especially the spleen and kidneys. 

Etiology. — It is met with most often in children and young adults 
(under 30 years) as the result of chronic suppuration such as occurs 
secondarily in tuberculosis and syphilis, especially in those forms of the 
disease involving the bones and lungs. It does occur in cachexias of 
other kinds, such as malignant disease, chronic malaria, etc., but rarely 
in those cases becomes of practical importance. 

Morbid Anatomy. — The liver is enlarged, sometimes enormously, 
its form preserved, the surface smooth and pale, the consistency in- 
creased, so that it is firmer and heavier than normal. The cut section 
is pale, and peculiarly translucent in appearance. Treated with iodine 
the section becomes mottled with areas stained deep brown — the amy- 
loid tissue. Microscopically the amyloid material is found particu- 
larly in the walls of the smaller arteries, and later in the capillaries and 
venules. 



130 



DISEASES OF THE DIGESTIVE SYSTEM 



Symptoms. — The patients are emaciated and anemic as the result 
of the primary trouble. The liver is greatly enlarged, may reach the 
level of the umbilicus or beyond it, smooth, firmer than normal, not 
painful or tender. The spleen is similarly enlarged, and usually there 
are evidences of like degeneration of the kidney, polyuria, with albumin 
in large amounts and waxy casts. Jaundice is absent. 

Diagnosis. — The sequence of protracted suppuration and painless 
enlargement of the liver, which is smooth but firmer than normal, is 
characteristic. From fatty liver it can be easily recognized by the asso- 
ciated changes in the spleen and kidney. 

Prognosis. — Amyloid degeneration is always a grave sign. The proc- 
ess is progressive and the end not long delayed. 

Treatment must be directed entirely to the primary condition. 



ANOMALIES IN FORM AND POSITION OF LIVER 

Malformations of the liver are either congenital or acquired. Con- 
genital malformation may consist of a disproportion in the size of lobes 
or in an increased lobulation: clinically it is unimportant. Acquired 
malformation results from (a) tight lacing. The right lobe is com- 
pressed by the lower ribs, and its anterior portion is forced downward 
and presents as a smooth, flat, pyramidal mass (Riedel's lobe) in the 
right hypochondrium, its edge sometimes reaching the level of the crest 
of the ilium. The line of pressure of the ribs may be marked only by 
a groove or by a dense band of cicatricial tissue which may form the 
only connection between the so-called Riedel's lobe and the rest of the 
organ, (b) Deformity of the vertebra? or ribs may change the shape 
of the liver. 

Symptoms are lacking, but the distorted liver forming a Riedel's 
lobe may easily be mistaken for a tumor of any of the adjacent 
viscera. Its form, consistency and connection with the liver, taken 
with the absence of symptoms and the sex of the patient, should distin- 
guish it. 

Displacements. — 1. Congenital. — Transposition of the liver is a 
rare condition, nearly always part of a complete transposition (situs 
transversus) of the heart, liver, spleen and other organs. 2. Acquired: 
The liver may be displaced (a) upward by ascites, abdominal tumors, 
or distention of the intestines; (b) do^vnward by pleuritic effusions, 
emphysema of the lungs, or intrathoracic tumors; (c) by relaxation of 
the ligaments, as in Glenard's disease, the liver is allowed to fall doAMi- 
ward and forward. 

Symptoms are usually lacking, except those resulting from pressure 
upon the adjacent organs. In downward displacements the organ may 
be mistaken for some form of abdominal tumor. Absence of dulness 
in the normal site and the ease with Avhich the organ can be replaced 
by pressure usually make its recognition easy. 



DISEASES OF BILE-PASSAGES AND GALL-BLADDER 131 



DISEASES OF THE BILE-PASSAGES AND 
GALL-BLADDER 

ACUTE CATARRH OF THE BILE-DUCTS 
(Catarrhal Jaundice. Acute Catarrhal Angiocholitis) 

Definition. — An acute catarrh of the common bile-duct causing 
obstructive jaundice. 

Etiology. — This affection is most frequently seen in young adults, 
but may occur at any age. It may be due to (1) Extension of catarrhal 
inflammation from the stomach and duodenum, caused by errors of diet, 
exposure to cold and wet, malaria, etc., into the common bile-duct. This 
is the usual cause. (2) Infectious fevers, such as pneumonia or typhoid 
fever. (3) Emotional disturbances. (4) Congestion due to disease of 
the heart, kidneys, or lungs. (5) It may occur as an acute infection in 
epidemic form. 

Morbid Anatomy. — Little is known of the pathology. We assume 
that it has the usual characters of catarrhal inflammation and that the 
common bile-duct, especially the terminal portion, is blocked either by 
swelling or by a plug of inspissated mucus. The liver may be enlarged 
and the gall-bladder distended. 

Symptoms. — The onset may be acute with moderate fever, 101° to 
102°, nausea, possibly vomiting, and prostration. Usually it is insidious 
with vague gastric disturbance, the cause of which is revealed by the 
development of the jaundice. Anorexia, nausea, or vomiting may pre- 
vail for several days or even a week before the jaundice. This presents 
the symptoms of obstructive jaundice, the icterus, bile-tinged urine, 
clay-colored stools, slow pulse, etc. Drowsiness and languor are usually 
pronounced. The liver and spleen may be slightly enlarged. The affec- 
tion lasts from two to four weeks, clearing up very gradually; in some 
cases it may be protracted to three months. 

Diagnosis.— This is the usual explanation of jaundice in young peo- 
ple. In older persons we must think of the other causes of obstructive 
jaundice, especially gall-stones and cancer. The short duration of 
catarrhal jaundice and the absence of pain or other symptoms are 
significant. 

Treatment. — Rest in bed is necessary only when the onset is severe. 
The diet must be suited to the gastric catarrh. Meats, fats, and sweets 
should be limited or excluded. The bowels require the use of laxatives, 
especially salines, such as sodiiun phosphate. Plain water or alkaline 
mineral waters may be given freely. Theoretically sodium salicylate or 
sodium bicarbonate may have a favorable influence by thinning the bile. 

CHRONIC CATARRHAL ANGIOCHOLITIS 
Etiology. — Chronic catarrhal angiocholitis is an accompaniment of 
chronic obstruction of the bile-ducts by stricture, tumor, pressure from 
without, or most frequently gall-stones. 



132 DISEASES OF THE DIGESTIVE SYSTEM 



Morbid Anatomy. — Behind the obstruction the bile-duets are dis- 
tended, their walls thinned or thickened by chronic inflammation. The 
contents consist of clear, sterile mucus, if the obstruction is complete; 
when the obstruction is partial only, the mucus is turbid, bile-stained, 
and yields on culture the colon bacillus or the ordinarj^ pyogenic cocci. 
The causative factor, such as gall-stones or tumor, is present. 

Symptoms. — When the obstruction is complete the symptoms are 
those of chronic obstructive jaundice. When incomplete the picture is 
modified by attacks of chills, fever, and sweating (secondary infection) 
lasting for days or weeks, mth intervening periods of freedom from 
fever. This so-called hepatic intermittent fever is most often caused by 
gall-stones. The blood shows a leukocytosis. 

Treatment. — This must be surgical, the removal of the obstruction. 

SUPPURATIVE AND ULCERATIVE ANGIOCHOLITIS 

Definition. — A general suppurative inflammation of the bile-ducts, 
usually accompanied by like conditions in the gall-bladder. 

Etiology. — There are regularly two factors. (1) Stagnation of bile, 
produced by some form of obstruction; (2) Infection with pyogenic 
organisms. Occasionally onh^ the latter cause is present, the affection 
following diseases such as pneumonia or tj^phoid fever. The pneiuno- 
coccus, the typhoid or colon bacillus, or the ordinary pyogenic organisms 
may be found in the pus. 

Morbid Anatomy. — The ducts and gall-bladder are distended, their 
walls thickened, the mucous membrane eroded, and they contain pus. 
Perforation of the distended ducts or gall-bladder may occur, with 
secondary peritonitis. 

Symptoms. — The clinical picture is that of a severe septic infection, 
wdth swollen and tender liA^er, enlarged gall-bladder, jaundice and a 
high leukocytosis. The distended gall-bladder may be palpable or we 
may only make out rigidity and tenderness to pressure of the overlying 
abdominal wall. 

Treatment is purely surgical. 

ACUTE INFECTIOUS CHOLECYSTITIS 

Definition. — An acute inflammation of the gall-bladder produced by 
bacterial invasion. The affection is similar to that just described, but 
limited to the gall-bladder. 

Etiology. — (1) j\Iost frequently gall-stones are present. (2) Pneu- 
monia or typhoid fever may precede the attack. In its genesis, as well 
as in its pathology and symptomatology, the disease presents a close 
analogy to appendicitis. 

Morbid Anatomy. — The gall-bladder is distended, its contents con- 
sisting of mucus, pus, and blood in varying proportions. There may be 
a localized peritonitis about the organ, or if its walls are perforated, an 



DISEASES OF BILE-PASSAGES AND GALL-BLADDER 133 



abscess or acute general peritonitis. The pneumococcus, typhoid or colon 
bacilli, streptococci or staphylococci may be found in the pus. 

Symptoms. — Sudden pain in the right side of the abdomen, followed 
by fever, rapid pulse, nausea and vomiting:, mark the onset. The 
abdomen becomes distended, rigid and tender in the gall-bladder region. 
Occasionally we may feel the distended gall-bladder. More often the 
rigidity forbids. There is no jaundice unless the common duct is in- 
volved. There is a high leukocytosis. In some cases the picture is much 
like intestinal obstruction with stoppage of gas and feces. 

Diagnosis. — The affection is most often mistaken for appendicitis or 
intestinal obstruction. From the former it can be differentiated only by 
its closer relation to typhoid fever or pneumonia, a knowledge of the 
presence of gall-stones, or ability to feel the distended gall-bladder. 
Localization of pain, tenderness and rigidity over the gall-bladder region 
are suggestive, but the appendix may, as we know, lie directly beneath. 
The acute inflammatory onset and the localization of the signs should 
exclude intestinal obstruction. 

Prognosis. — The milder cases recover within a week under palliative 
treatment. Severer infections go on to suppuration and may result 
fatally from sepsis or from secondary peritonitis. 

Treatment. — For the milder conditions the application of an ice-bag 
over the gall-bladder and the relief of abdominal distention by enemata 
or stupes seem sufficient. If suppuration occurs, the incision and drain- 
age of the gall-bladder or its complete removal may be necessary. The 
total leukocyte count and the differential are helpful indications of the 
development of suppuration as in appendicitis. 

CHOLELITHIASIS 

Etiology. — There are two essential factors in the production of gall- 
stones: (1) A catarrhal inflammation of the gall-bladder. (2) An ob- 
struction to the free outflow of bile. Gall-bladder inflammation is 
excited most often by typhoid or colon bacilli, less frequently by the 
ordinary pyogenic organisms. A previous history of typhoid fever 
or other acute infectious disease is therefore frequent in cholelithiasis. 
Stagnation of bile is brought about by a sedentary life, lack of exercise, 
relaxation of the abdominal muscles, such as follows repeated pregnan- 
cies, or in women by tight lacing. While much influence has been at- 
tributed to dietetic errors with consequent disturbances of metabolism, 
there is at present no clear evidence that diet has any direct influence 
upon the formation of gall-stones. Practically cholelithiasis is met with 
most frequently in women, and usually in those over 40 years of age. The 
proportion of women to men affected may be- as high as 5 to 1 . Seventy- 
five per cent, of the cases occur in people over 40 years of age and but 1 
per cent, in those under 20. 

Morbid Anatomy. — Gall-stones may occur singly, but usually are 
multiple and may number thousands. They vary in size from minute 



134 



DISEASES OF THE DIGESTIVE SYSTEM 



granules to several inches in diameter ; stones weighing 135 grammes are 
on record. In form they are usually round and smooth, but they may 
be of various shapes. When multiple they are facetted by friction upon 
one another. Most of them are quite soft and crumble readily when 
dried, but some are hard. Large numbers of stones are commonly found 
in the gall-bladder, the cystic or common duct, or the intestines. Rarely 
stones are found in the hepatic duct or even in the liver. Sometimes 
they may be found outside the biliary tract, in adhesions, abscesses, etc. 

Composition of Gall-Stones. — The stones consist chiefly of choles- 
terin, bile-pigments, and calcium carbonate. The eholesterin is not de- 
rived from the bile, but from the degeneration of the cells lining the 
gall-bladder. The pigments and calcium salts are derived from the bile 
itself. The proportion of these several ingredients varies in different 
stones, but the chief constituent is the eholesterin. 

Associated Lesions. — Wherever gall-stones lodge, their presence is 
associated with some degree of inflammation, catarrhal or suppurative, 
rarely gangrenous. Thus in the gall-bladder or bile-passages there 
may be any degree of cholecystitis or cholangitis with their possible 
results. In some instances the inflammatory process involves the peri- 
toneum and dense adhesions form about the gall-bladder or biliary tract, 
or in the severer cases there may be localized collections of pus or even 
a general peritonitis, from rupture of the bile-passages or gall-bladder. 

Obstruction may be the chief result of the presence of gall-stones. 
Either the cystic, or the common duct, or, with very large stones, the 
intestine may be blocked. If the cystic duct is blocked, the gall-bladder 
becomes distended, possibly acutely inflamed. In rare instances it 
atrophies. With the obstruction of the common duct, obstructive jaun- 
dice develops. When the stone lodges in the intestine, obstruction of 
that part results. 

Symptoms. — These depend upon two factors: (1) The situation of 
the stone or stones; (2) the presence or absence of secondary infection. 
The stones may be in the gall-bladder, the cystic or common duct, the 
papilla of Yater, or the intestine. The secondary infection may be of 
the mildest grade, giving evidence of its presence only by the slightest 
fever and constitutional disturbance at the time of attacks of biliary 
colic or in the intervals between such attacks, or by symptoms of infec- 
tion of more marked type, rising at times to the picture of acute sepsis. 
The situation of the stones does not determine the severity of the infec- 
tion, but stones in the gall-bladder may be accompanied by violent infec- 
tions as readily as those in the common duct, or in the papilla of Yater. 
The results of the combination of the two factors, the mechanical pro- 
duced by the presence of stones, and the infective, are clinical symp- 
toms of remarkable variety and complexity. In most cases stones are 
found both in the gall-bladder and in other parts of the biUary tract. 

Stones in the Gall-Bladder, — The gall-bladder may be full of 
stones without producing symptoms, the stones being found at autopsy. 
In the great majority of cases, however, symptoms result either from 



DISEASES OF BILE-PASSAGES AND GALL-BLADDER 135 



efforts of the gall-bladder to expel the stones, resulting in the classical 
gall-stone or biliary colic, or secondary infections and inflammation of 
the gall-bladder. 

Biliary Colic. — The onset is sudden, the pain is sharp and severe, 
referred usually to the right hypochondrium, sometimes to the epigas- 
trium, frequently radiating to the back under the right scapula or into 
the right shoulder, lasting from one or two hours to twelve hours, and 
followed in many cases after a few hours or a day or two by jaundice. 
Vomiting regularly occurs at the onset and may be repeated. Relief 
comes either from the stone dropping back into the gall-bladder or from 
its passage through the ducts into the intestine. In the first case there 
should be no jaundice, in the second jaundice is excited by the mechan- 
ical obstruction caused at first by the stone itself, later by swelling of 
the ducts due to traumatism and possibly secondary inflammation. 
During the attacks there is usually fever, 101° to 103° F., the pulse is 
rapid, and the patient is prostrated. Fever may be altogether absent. 
With the subsidence of the pain, recovery is rapid, unless the attack 
ushers in some of the more remote consequences. These attacks of pain 
are repeated at intervals of weeks, months or years, depending upon the 
number of stones present and the efforts of the gall-bladder to eject 
them. A single attack is a possibility. Repeated attacks regularly im- 
pair the nutrition and general health so much as to demand surgical 
intervention to remove the stones. 

With stones in the gall-bladder we may have acute or chronic chole- 
cystitis, with the symptoms already described. The chronic cases are 
peculiarly likely to be mistaken for dyspepsia or gastritis. The abse-nce 
of jaundice makes such errors easy. In certain cases even after the 
escape of the gall-stones the chronic inflammation of the gall-bladder, 
especially when associated with dense adhesions to the surrounding vis- 
cera and abdominal wall, may continue to give symptoms. 

Gall-Stones in the Cystic Duct. — If the obstruction is complete, 
the gall-bladder first becomes distended, the bile in it is replaced by 
clear mucus and ultimately it atrophies and may be reduced to a fibrous 
mass. If the obstruction is not complete, infective processes develop, and 
the patient suffers from acute or chronic cholecystitis. 

Gall-Stones in the Common Duct. — The results depend in part 
upon the completeness of the obstruction. If complete, the symptoms 
are those of obstructive jaundice with or without inflammation of the 
gall-ducts and bladder. (See Cholangitis and Cholecystitis.) Not 
infrequently in these cases chronic obstructive jaundice is the only 
symptom. If the obstruction is incomplete, there may be no jaundice 
at all, or the stone may act as a ball-valve and produce jaundice with 
periods of remission and exacerbation. Under these conditions secondary 
infective phenomena are common and the patient suffers from chronic 
catarrhal or suppurative inflammation of the ducts or the bladder. The 
latter is the more common and characteristic. With such suppurative 
inflammation in the gall-passages we may find the so-called hepatic 



136 



DISEASES OF THE DIGESTIVE SYSTEM 



intermittent fever of Charcot. By this is meant not intermittent fever 
as commonly understood, but periods of fever, either continuous, remit- 
tent or intermittent in type, followed by periods of normal temperature. 
Increase in the jaundice regularly accompanies the return of the fever, 
as the swelling of the ducts caused by the increasing inflammation more 
completely blocks them. In this connection must also be cited the 
so-called law of Courvoisier. It is not by any means a law, but an 
observation to the effect that obstruction of the common duct by stone 
is not followed by dilatation of the gall-bladder, while such dilatation 
does occur in other forms of chronic obstructive jaundice, such as are 
produced by tumors in the head of the pancreas, the pressure of tumors 
upon the ducts, etc. The observation is of help, but like all other obser- 
vations of this kind it is subject to exceptions. 

Gall-Stones in the Papilla of Vater. — For the most part the con- 
ditions are the same as with stones in the common duct. Stones in the 
papilla may, however, block the duct of Wirsung, and thus produce 
accumulation of the pancreatic juice with dilatation of the ducts and 
possibly a cyst of the pancreas, if the ducts of Santorini are not so sit- 
uated as to relieve the stoppage. Secondarily chronic inflammation of 
the head of the pancreas, or pancreatic lithiasis may be met with. If 
the obstruction of the pancreatic duct is incomplete, bile may be diverted 
into the pancreas and acute hemorrhagic pancreatitis set up. It ^^dll 
thus be seen that gall-stones may be the cause of important secondary 
disease of the pancreas. Mayo found gall-stones present as an accom- 
paniment in 81 per cent, of 168 operations for disease of the pancreas. 

Diagnosis. — Of Biliary Colic. — The diagnosis of the presence of 
gall-stones often rests on the recognition of attacks of colic. These are 
identified by the location of the pain, its sudden onset, radiation to the 
back and shoulder, brief duration, rapid subsidence, and the subsequent 
jaundice, if present. Jaundice is, however, often missing. In doubtful 
cases if the feces for 48 hours after the attack are collected and washed 
through a sieve, the stones may rarely be recovered. Biliary colic must 
be distinguished from renal colic, gastralgia, gastric ulcer, and appen- 
dicitis. If the appendix chance to be located immediately beneath the 
gall-bladder, an operation may be required to complete the diagnosis. 

The diagnostic features of cholecystitis have already been given. In 
this connection a history of previous gall-stone attacks is of the greatest 
value. 

Gall-stones in the common duct commonly produce jaundice, and 
must then be differentiated from the various other causes of obstructive 
jaundice. If jaundice be not present the diagnosis is often extremely 
difficult. The frequency with which repeated attacks of indigestion in 
both men and women over 40, but especially the latter, are found to be 
due to gall-stones must be remembered. Chronic inflammatory lesions 
of the neighboring viscera, especially the liver, kidney, pancreas, or 
peritoneum, must be considered. Oftentimes operation alone clears up 
the diagnosis. 



DISEASES OF THE PANCREAS 



137 



Prognosis. — Gall-stone colic alone is rarely fatal. One attack may 
be the last, but usually the attacks are repeated. Danger to life arises 
from the complications, obstructive jaundice, cholecystitis and cholan- 
gitis. Where jaundice accompanies the cholecystitis or cholangitis the 
prognosis, in case of operation, is always grave by reason of the tendency 
to hemorrhage. Otherwise the danger is in proportion to the severity 
of the inflammation, i.e., it is greater if pus be present. 

The Blood. — The leukocyte count in gall-stone colic will show slight 
increase or remain normal. If cholecystitis or cholangitis develop, the 
leukocytes are increased usually in proportion to the severity of the 
process. If pus be present, the percentage of polymorphonuclears may 
be increased to 85 per cent, or 90 per cent. 

Treatment. — For gall-stone colic the surest relief is had from the 
hypodermic injection of morphine sulphate, one quarter to one-third 
grain. Chloroform may be given sufficiently to dull the pain. Hot 
fomentations to the gall-bladder region are grateful. After the attack 
we must face the problem of preventing further attacks or the formation 
of more stones. The patient must be given an easily digestible diet. 
As already explained, the cholesterin does not come from the food, nor 
has the composition of the food much influence upon the biliary secretion. 
The diet is therefore to contain proteids, fats, and carbohydrates in 
reasonable proportions and in forms tending to their ready digestion. 
A'^hu.iine waters are given freely. Exercise is required, especially such 
as bring the abdominal muscles into play. The bowels must be kept 
open, by laxatives if necessary. Sodium phosphate or sulphate may be 
given in one to two dram doses in a glass of water each morning. For 
repeated attacks of gall-stone colic or for the severer complications of 
gall-stones surgical intervention is necessary. The milder forms of 
these affections may yield to rest in bed, regulation of the diet, relief 
of constipation, and the local application of an ice-bag. 

DISEASES OF THE PANCREAS 

I. ACUTE PANCREATITIS 

ACUTE HEMORRHAGIC PANCREATITIS 
Etiology. — The disease occurs most often in men, especially those 
over forty. But two definite causes are known: (a) Trauma, such as 
blows upon the abdomen, and (b) obstruction of the papilla of Vater 
by gall-stones so that bile is forced into the pancreatic duct. In many 
cases no satisfactory cause is found. Bacterial invasion, especially by 
the bacillus coli, can often be demonstrated, but is probably secondary. 

Morbid Anatomy. — ^The pancreas is enlarged, firm, dark-red, and 
marbled by the mingling of hemorrhagic areas and normal tissue. The 
interstitial tissue is infiltrated with blood, the organ ruptured in places, 
and the blood infiltrates the retroperitoneal tissue and forms a more 
or less extensive hemorrhage, in some cases extending even into the 
pelvis. The peritoneum may contain bloody serum. The subperitoneal 



138 



DISEASES OP THE DIGESTIVE SYSTEM 



tissue of the abdominal walls, the mesocolon, the mesentery, and retro- 
peritoneal fat, show areas of fat necrosis. Microscopically the pancreas 
shows more or less extensive necrosis, and hemorrhage, and in places an 
inflammatory exudate of leukocytes and fibrin. If the course of the 
disease is protracted to a fortnight or longer the pancreas and adjacent 
tissues may be found gangrenous. 

Symptoms. — The disease may attack robust men or occur in those 
who have suffered attacks of pain due either to gastric disturbances or 
gall-stone colic. (See pp. 136-137.) The onset is sudden, marked by 
severe abdominal pain, referred to the epigastrium, nausea and vomit- 
ing. The abdomen, especially the epigastric region, becomes distended, 
exquisitely tender, and t;sTiipanitic. Symptoms of collapse develop 
rapidly. The patient is profoundly prostrated, pale, the respiration 
rapid and deep (air-hunger), the pulse rapid and feeble. The tem- 
perature may be either normal, subnormal, or elevated. The bowels 
are usually constipated, but may be loose. In most cases death occurs 
within one or two days in sjTicope or coma. Glycosuria is rarely found. 

Gangrenous pancreatitis is now recognized only as an advanced 
stage of the acute form. If the patient survives three or four days, the 
pancreatic tissues may become gangrenous, and an abscess cavity form 
in which lies more or less of the necrotic organ. 

Symptoms. — The violent pains of the onset subside, the patient 
develops fever, sweating, rapid pulse and other signs of bacterial inva- 
sion. The abdomen continues distended and tender and a mass may be 
made out in the epigastric region. Jaundice may develop, and glyco- 
suria is occasionally found. In two cases the separated pancreas has 
been discharged per rectum. 

The BLOOD shows a leukoc>d:osis, sometimes quite high, 30,000 or over. 

Diagnosis is difficult. The s^nnptoms very closely resemble those 
of acute peritonitis following the perforation of a gastric ulcer, or those 
of intestinal obstruction. If the hemorrhage be large enough to give 
the typical signs of bleeding, the diagnosis may be easy. 

Treatment. — For the violent pain morphine may be given hypo- 
dermatically or chloroform by inhalation. The colon may be emptied by 
enemata and stimulating injections given. H}T)odermoclysis may be 
helpful in prolonging life. Surgical treatment offers the only hope of 
meeting the conditions satisfactorily. 

SUPPURATIVE PANCREATITIS 

Etiology. — Suppuration may follow acute hemorrhagic pancreatitis 
or may be primary. Infection takes place either through the blood ves- 
sels or ducts. In the latter case, suppuration is greatly favored by 
obstruction of the duct of Wirsung by gall-stones, cyst, or cancer of 
the pancreas. It is met with especially in men over forty. 

Morbid Anatomy. — The abscess may be either in the substance of the 
pancreas or in the surrounding tissues. The cavity of the lesser peri- 
toneum may be involved in the process. 



DISEASES OF THE PANCREAS 



139 



Symptoms. — The onset may be that of acute hemorrhagic pancre- 
atitis or it may be gradual with a history of pain in the epigastrium and 
disturbance of digestion. Only when suppuration is well established, 
after four or five days, is the clinical picture definite. (1) The consti- 
tutional picture is that of sepsis with fever, rapid pulse, sweating, 
anemia, and emaciation. These symptoms may be slight or very marked. 
(2) The local signs include distention of the epigastrium with pain, ten- 
derness, rigidity, and possibly an ill-defined tumor lying behind the 
stomach. Only in rare cases can the tumor be made out definitely. 
Glycosuria or fatty diarrhea is rare. 

Course. — The duration may be a few days or several months. Event- 
ually the abscess bursts into one of the ad.jacent organs or into the 
peritoneum. General peritonitis may result from such rupture or may 
be caused by extension without rupture. 

The BLOOD shows a leukocytosis, with possibly an increased percentage 
of polynuclear cells. 

The DIAGNOSIS in the acute stages cannot be made from the acute 
hemorrhagic type. In the more chronic cases the constitutional symp- 
toms of sepsis with the indefinite tumor in the epigastrium may identify 
the affection. Such symptoms are of special import if developed subse- 
quently to cholelithiasis, cancer or cyst of the pancreas. 

Treatment is purely surgical. 

CHRONIC PANCREATITIS 

A chronic interstitial inflammation of the pancreas, rarely recog- 
nized during life, found frequently at autopsy, and of interest chiefly 
by reason of its relation to diabetes and of the possibility of mistaking 
it for carcinoma. 

Etiology. — (1) Obstructions of the pancreatic duct caused by cal- 
culi, either pancreatic or biliary, cysts, or cancer of the gland. (2) 
Arteriosclerosis, especially that produced by alcohol. In this relation 
it may accompany cirrhosis of the liver. 

Morbid Anatomy. — The pancreas is of normal size or contracted, 
firm, dense on section. The increased fibrous tissue may be plainly seen. 
Small cysts may be formed in the gland. Microscopically the increased 
fibrous tissue is found to be either interlobular or interacinar. In the 
former case the islands of Langerhans are preserved, in the latter they 
are atrophic, possibly fibrous. 

Symptoms. — Gastric and intestinal indigestion are present, some- 
times with attacks of pain, fever and vomiting. The stools may show 
abundance of fat and undigested muscle fibre, and in severe cases of the 
interacinar type diabetes may develop. The urine may give Cammidge's 
reaction. Not infrequently at operations for gall-stones the head of 
the pancreas is found so hard and seemingly enlarged that it is thought 
to be cancerous, but observation or autopsy proves the condition to have 
been chronic pancreatitis. The possibility that such glands may be felt 
as abdominal tumors in thin persons must be admitted. 



140 



DISEASES OF THE DIGESTIVE SYSTEM 



PANCREATIC CYST 

Etiology. — A rare form of abdominal tumor, seen in adult men and 
women. It may be caused (a) by trauma; (b) by obstruction of the 
pancreatic duct due to stone, tumor, or pressure from without; (3) 
by proliferation of the epithelial tissue of the gland. 

Morbid Anatomy. — The cyst forms a round or oval tumor in the 
upper abdomen, presenting either above the stomach, between stomach 
and colon, or below the colon. The contents may be clear and watery, 
or viscid and brownish from the presence of mucus and blood. ]Micro- 
scopically the fluid shows epithelial cells, leukocytes, some of them 
containing fat, crystals of fatty acids, and altered red cells. 

The fluid may show the presence of tryptic, diastatic, and emulsi- 
fying ferments ; most often the diastatic only is found. 

Symptoms. — (1) The tumor is the essential symptom. It presents 
as a smooth, round or oval mass in the epigastrium, but slightly tender 
or painful, either movable or fixed; fluctuation may be detected, only if 
the tumor is near the surface. It may be above or beloAV the stomach, 
possibly even below the colon. The tumor may be to right or left of 
the median line, or even in the region of the left kidney, depending upon 
the portion of the pancreas from which it arises. It may be small or 
large enough to fill the abdomen. (2) Glycosuria or fatty stools from 
interference with the function of the gland are rare. ( 3 ) Pressure symp- 
toms develop, if the tumor be large, abdominal discomfort or pain 
referred to the epigastrium; disturbances of the digestion, such as loss 
of appetite, pain after eating, nausea or even vomiting; in case the 
tumor arise from the head of the pancreas jaundice may be caused, or 
ascites from pressure on the portal vein. (4) Loss of weight and weak- 
ness are generally noted. These cysts may empty spontaneously into the 
intestine and later refill. Traumatic rupture into the peritoneum may 
occur. 

Diagnosis rests upon the physical signs of the character and location 
of the tumor. Distention of the stomach and colon aid in the location. 
The tumor must be differentiated from an enlarged gall-bladder, cysts 
of the omentum, hydronephrosis of the left kidney, and in case of very 
large tumors from ovarian cysts. 

Treatment is purely surgical. The cyst must be opened and drained. 

CARCINOMA OF THE PANCREAS 

Etiology.- — Cancer of the pancreas occurs in middle life, in men 
more often than in women. It may be primary or secondary to cancer 
of adjacent organs, especially the stomach. 

Morbid Anatomy. — The tumor most frequently occurs in the head 
of the pancreas, but may occupy any part. The cancer is usually very 
hard, scirrhous in type, but may be soft or encephaloid, or colloid. The 
gland is more or less enlarged, especially the head, dense and hard. On 



DISEASES OF THE PANCREAS 



141 



section the increased fibrous tissue is evident and also gray areas repre- 
senting the cancerous infiltration. Sharply outlined tumors are rare. 

Symptoms. — The development of the new growth is marked by 
indefinite symptoms of digestive disturbance, loss of appetite, distress 
after eating, eructations, nausea or even vomiting. After these symp- 
toms have existed for some weeks or months the patient develops the 
general symptoms of cancer, pain, cachexia, and tumor. (1) The pain 
is referred to the abdomen, radiating into the shoulders or back. It is 
more or less constant. (2) The cachexia is marked, loss of both weight 
and strength being rapid. (3) A tumor may not be palpable for some 
time, in some cases not at all. Long before it is palpable it gives evi- 
dence of its presence by obstructing the common bile-ducts and causing 
jaundice. The jaundice in these cases deepens steadily till it becomes 
most intense, and so continues. The gall-bladder may be distended. If 
palpable the tumor presents most often in the epigastrium, rarely in 
either hypochondrium. It is hard, tender, and fixed or but slightly 
movable. Remote evidences of involvement of the pancreas may be 
found in glycosuria or rarely in the occurrence of fatty stools. The 
temperature is usually normal or below; fever is rarely seen. 

Diagnosis. — The age of the patient, the pain and cachexia, increas- 
ing jaundice, and the epigastric tumor are most important. Before the 
appearance of the tumor the diagnosis from gall-stones is difficult. The 
history of previous colic, variability of the jaundice, absence of enlarge- 
ment of the gall-bladder (Courvoisier 's law), and presence of fever 
point to gall-stones. Severe pain, rapid emaciation, steadily increasing 
jaundice, and distention of the gall-bladder belong to cancer of the 
pancreas. Glycosuria or fatty stools aid the diagnosis in some cases. 
The development of a tumor usually settles the question. Cancer of the 
pancreas must be distinguished also from cancer of stomach or gall- 
bladder. Chronic interstitial pancreatitis is occasionally at operation 
TPistaken for cancer. 

Treatment must be purely symptomatic. 

PANCREATIC CALCULI 

These are exceedingly rare. Only seven cases in which the diagnosis 
has been made during life are on record. Pancreatic calculi are doubt- 
less produced by causes similar to those acting in cholelithiasis, infection 
and obstruction. They may therefore accompany tumors and other 
forms of obstruction. The symptoms, if any be present, cannot be dis- 
tinguished from those of biliary colic, except by the recovery of the 
stones. These are found to consist almost wholly of calcium salts, the 
carbonate and phosphate, without bile-salts or pigment. The treatment 
of the condition is purely symptomatic. 



142 



DISEASES OF THE DIGESTIVE SYSTEM 



DISEASES OF THE PERITONEUM 

ACUTE GENERAL PERITONITIS 

Definition. — An acute inflammation of the peritoneum. 

Etiology. — This disease may be either primary or secondary. (1) 
Primary: The possibility of a primary peritonitis is admitted by all 
writers, but it is so rare as to be practically negligible. Exposure to cold 
and wet, and rheumatism are said to cause it. (2) Secondary: The 
peritonitis is here due to infection, pathogenic organisms being admitted 
either from without, or from the viscera covered by the peritoneum or 
in close relation thereto, or in rare instances from the blood, (a) 
Wounds or operations involving the peritoneum are common causes, 
especially if they at the same time involve any of the hollow viscera, 
particularly the stomach or intestines, (b) Perforation by ulceration or 
new growth of the stomach, intestine, appendix or other hollow viscus, 
discharging its contents into the peritoneum, or rupture of an abscess 
of the appendix, gall-bladder, liver, spleen, kidney, tubes, or uterus, or 
any part of the abdominal cavity into the peritoneum, (c) Extension 
of inflammation without actual rupture in any of the conditions just 
given. In cancer of the stomach or intestine, in appendicitis, etc., 
peritonitis may develop from extension alone. In rare instances the 
inflammation may extend from the pleura or pericardium. Apart from 
direct wounds, operative or accidental, acute peritonitis most frequently 
develops in men from appendicitis, in women from infection through the 
uterus, tubes and ovaries, from gastric ulcer, or from appendicitis. 
Acute peritonitis may also be found as a terminal complication in 
Bright 's disease, arteriosclerosis, or gout. 

Bacteriology. — The organisms found include a wide variety. The 
colon bacillus is regularly present when the infection arises from the 
alimentary tract, either alone or combined with other bacteria. When 
abscesses or suppurations of other viscera are the source, streptococci or 
staphylococci may be expected. Many other organisms m.ay be found 
usually accompanying these common invaders, rarely alone, such as the 
pneumococcus, bacillus proteus, bacillus pyocyaneus, bacillus tubercu- 
losis, bacillus aerogenes capsulatus. bacillus typhosus, and gonococcus. 

Morbid Anatomy. — The peritoneum is congested, its surface dull 
and coated with an exudation of fibrin. This may be sufficient only to 
render the surface granular or may be abundant, gluing the intestinal 
coils and other parts of the peritoneum together and showing as a thick 
pellicle. Fluid accumulates in the peritoneum, usually in small quan- 
tity, but sometimes to the amount of several quarts. It is serous, sero- 
fibrinous, or purulent; in rare cases hemorrhagic. Especially in infec- 
tions from the intestinal tract the exudate presents a very foul odor 
from the presence of putrefactive bacteria. 

Symptoms. — The onset varies greatly. In cases of perforation as 
in typhoid fever there may be an initial fall of temperature to normal or 



DISEASES OF THE PERITONEUM 



143 



below, quickly followed by a rise to 103° or 104°. In other cases the 
onset may be marked by a chill and rapid rise of temperature, or the 
onset may be insidious with very little fever. Pain in the abdomen is 
often the first symptom, sudden, sharp, severe and continuous. Tender- 
ness regularly develops with it. Nausea and vomiting follow, and the 
vomiting is repeated, the vomitus being first gastric contents, then mucus, 
and finally bile-stained (greenish) material from the intestine. The 
bowels are constipated, rarely loose. With these symptoms the patient 
is greatly prostrated, the pulse rapid, small, and hard, the respiration 
shallow and somewhat rapid, the face showing suffering and anxiety. 
After the onset there may be a temporary improvement in the symp- 
toms, but this is soon followed by their return in increasing severity. 
The temperature may be low, not over 101° F., but usually rises steadily 
to 104°-106° F. The pulse grows more and more rapid, 140 to 150 per 
minute, harder and more thread-like ; the respiration more shallow and 
hurried. The facies becomes drawn, the eyes sunken and dark-ringed, 
the color ashen or livid — the so-called Hippocratic facies. The vomiting 
persists, the abdomen continues tender and painful and gradually be- 
comes more and more distended. Constipation is marked. There may 
be frequent urination, difficulty in passing the urine or retention. The 
urine is scanty and contains a trace of albumin, possibly casts, and 
much indican. The mind is usually clear until death, but in typhoid 
fever the patient may be so dull that he complains of no pain and never 
realizes the change in his condition. 

Physical Signs. — The patient lies upon his back with the knees 
drawn up to relax the abdomen. The abdomen is held rigid, the thorax 
only moving in respiration. At first the abdomen is sunken, later dis- 
tended. There is a general muscular rigidity with exquisite tenderness. 
At the onset the location of the pain, rigidity or tenderness is most 
marked at the site where the process began, e.g., about the stomach or 
appendix. When the abdomen is distended, it is markedly tympanitic. 
Late in the disease there may be sufficient fluid in the flanks to give mov- 
able dulness. If gas is present in the abdominal cavity, as from rupture 
of the stomach or intestine, the liver dulness may be notably diminished 
or absent, a sign often emphasized, but sometimes seen in other condi- 
tions as well. If the abdomen is distended the liver dulness and also 
the situation of the apex of the heart may be displaced upward. 

Course and Prognosis. — The disease is regularly progressive and 
swiftly fatal. A patient with perforation during typhoid fever usually 
survives not more than 24 or 48 hours. In other conditions the duration 
is longer and the patient may live a week. Unless relief is secured by 
operative procedure, death is regularly the outcome. Recovery is, 
however, possible, especially in gonococcus or pneumococcus infections. 

The BLOOD shows, as a rule, leukocytosis which may be quite high, 
20,000-30,000, but this sign may be lacking in the severest cases, espe- 
cially after perforation in typhoid fever. 

Diagnosis. — The combination of the constitutional and local signs is 



144 DISEASES OF THE DIGESTIVE SYSTEM 



usualh^- characteristic. Intestinal obstruction or acute pancreatitis may 
give a clinical picture which is hardly distinguishable. Error in these 
cases is not important, for operative interference is called for as much 
as in acute peritonitis. Great clilBculty may be met in certain cases 
of localized peritonitis, appendical or pelvic, in excluding general peri- 
tonitis. The localization of the signs and the general condition of the 
patient are most important. A few hours' observation with expectant 
treatment usually leads to a correct conclusion. The greatest difficulty 
is met with in determining the presence of acute peritonitis following 
perforation in typhoid fever. The mental condition of the patient often 
prevents complaint of pain and tenderness. We must then rely upon 
evidence of a sudden change for the worse in the patient's condition and 
rapid change in the abdominal condition, with the presence of general 
rigidity, distention, and possibly fluid in the flanks. Obliteration of 
liver dulness is suggestive but not conclusive. Hysteria is said at times 
to give most deceptive signs of peritonitis. A normal blood count would 
here be most suggestive. 

Treatment. — Symptomatic treatment may be employed till such time 
as the diagnosis is established. Persistent vomiting requires the cessa- 
tion of mouth feeding, or the giving of food and water in teaspoonful 
quantities at frequent intervals. Peptonized milk is the best nutriment. 
If these measures fail, washing out the stomach may give relief. The 
bowels are emptied by enemata, and if the distention is marked a rectal 
tube is kept constantly in place, while turpentine stupes are applied to 
the abdomen. Cardiac stimulants are required and those which can be 
given hypodermatically are to be preferred, such as digitalin, strych- 
nine, caffeine, and camphor. The severe pain may call for the use of 
morphine hypodermatically, but in the initial stages the administration 
of morphine is always most ob.jectionable, because it so masks s^miptoms 
as to frequently mislead the observer, and delay the recognition of the 
gravity of the disease. When the diagnosis is settled and the course of 
action clear, that objection no longer holds. The practice of giving 
saline purgatives with the purpose of draining the peritoneum through 
their action has been given up. As soon as the diagnosis is established 
the condition must be treated surgically. 

LOCALIZED PERITONITIS 

Various parts of the peritoneum may be involved in a localized 
peritonitis. Thus the spleen is frequently bound do^\Ti by adhesions 
representing a previous peritonitis, or the liver or gall-bladder may be 
similarly affected. In women the pelvic organs are most often involved. 
Most frequently these localized processes are incidents of a major proc- 
ess, such as uterine inflammation or salpingitis, cholecystitis, etc., but 
occasionally the localized peritonitis becomes of considerable importance. 
Three principal forms may be described, depending upon the localization 
of the disease — pelvic, appendical, and subphrenic. 



DISEASES OF THE PERITONEUM 



145 



Pelvic peritonitis is secondary to disease of the uterus or tubes. 
It may be septic, gonorrheal or tubercular. It is at first localized and 
usually remains so, but may become general, or may give rise to abscesses 
which later rupture into the peritoneum and excite a general process. 
With the subsidence of pelvic peritonitis adhesions and thickening of 
the peritoneum are left and persist for years, possibly for life. 

Appendical peritonitis is a similar process localized about the 
appendix. It is regularly part of the several varieties of appendicitis, 
and is produced ordinarily by extension of the inflammation through 
the wall of the appendix. The abscesses so often found about the 
appendix are produced in this way. These abscesses remain localized 
or in some cases rupture into the peritoneum. The adhesions so often 
found about the appendix are evidences of previous local peritonitis. 

The symptoms and treatment of pelvic and appendical peritonitis 
cannot be separated from those of the underlying condition. 

Subphrenic Peritonitis, Subphrenic Abscess or Subphrenic Pyo- 
pneumothorax. — A rare form of localized peritonitis involving the 
peritoneum covering the diaphragm and liver, in some cases possibly 
the lesser peritoneal sac. 

Etiology. — Primary cases are said to follow injury, but are exceed- 
ingly rare. The usual causes are: (1) Extension from abscess of the 
liver, gall-bladder, right kidney, or appendix. (2) Extension from the 
pleura. (3) Perforation of a gastric or intestinal ulcer. In these cases 
air or gas as well as pus is found in the abscess. 

Morbid Anatomy. — The abscess on the right lies between the upper 
surface of the liver and the diaphragm, on the left between the 
diaphragm and the stomach and spleen, possibly in the lesser peritoneal 
cavity. The contents consist of pus alone, or in cases arising from 
perforation of the stomach or intestine, pus with air or gas and even 
food. 

Symptoms. — The genera] symptoms are those of suppuration, fever, 
either low or high, rapid pulse, sweating, anemia, prostration and 
emaciation. From upward displacement of the diaphragm or involve- 
ment of the pleura dyspnea may be severe. Local pain and tenderness 
may be marked. 

Physical Signs. — (1) Downward displacement of the liver, if the 
abscess is right-sided. (2) Enlargement of the thorax. (3) Dulness 
corresponding to the area of the abscess, or, if air be present, the signs 
of pneumothorax. (4) If the abscess be on the left side, it may form a 
tumor in the epigastrium. 

Diagnosis. — Subphrenic abscess is often mistaken for empyema, or 
abscess of the liver, or in the gaseous cases for pyopneumothorax. The 
condition in the milder forms may be easily overlooked. The aspirating 
needle is of great aid in locating the pus. For differentiation emphasis 
must be put on (1) previous history of disease of appendix, gall-bladder, 
stomach or other source of infecti(m below the diaphragm. (2) Ex- 
amination by X-rays, which may locate the diaphragm above the abscess. 
10 



146 



DISEASES OP THE DIGESTIVE SYSTEM 



(3) Pfuhl's sign: If an aspirating needle is in the abscess, the flow of 
pus is not interrupted by inspiration, as it is in empyema. (4) Fur- 
bringer 's sign : If an aspiratory needle is introduced into a cavity above 
the diaphragm no movement occurs in respiration. If the needle passes 
through the diaphragm the outer end moves up in inspiration and do^vn 
in expiration. 

Prognosis. — Unless recognized and drained these abscesses are always 
fatal. In some cases death ensues even after the abscess has been 
drained. 

Treatment is purely surgical. 

CHRONIC PERITONITIS 

Chronic peritonitis is of pathological rather than of clinical interest. 
It is frequently seen in one form or another post-mortem, rarely recog- 
nized during life. Several forms are described. 

Local Adhesive Peritonitis. — Local inflammations of the peritoneum 
are common during life, about the uterus and tubes, the appendix, the 
liver, spleen, or gall-bladder. As a sequel the peritoneum in any of 
these localities may be found thickened and adherent. Such adhesions 
may give rise to occasional twinges of pain during life ; occasionally they 
become important by contracting in such a w^ay as to obstruct the bowel, 
or interfere with the functions of the stomach, or other viscera. 

General adhesive peritonitis is frequently found in association 
with hepatic cirrhosis or chronic congestion. The peritoneum is every- 
where thickened, opaque, and adherent, the coils of intestine every^vhere 
matted together, and adjacent viscera bound doAvn to such an extent that 
the cavity may be obliterated. In other cases a serous effusion of con- 
siderable amount may be present. Such chronic peritonitis may be one 
factor in the recurring ascites of cirrhosis or chronic congestion. Occa- 
sionally the contents of the sac become purulent. We may suspect such 
a condition where an ascites requires frequent tapping, but cannot 
prove it. 

Proliferative peritonitis is also associated with cirrhosis or chronic 
congestion, and is very much like the preceding except that in this 
condition in addition to the general thickening and the serous effusion 
there are masses consisting of thickened omentum or folds of peritoneum 
and coils of intestine, the mesentery or mesocolon. These masses may 
form veritable tumors. Under these conditions tubercular peritonitis 
would be suspected, but the fluid if removed is found not to contain 
bacilli or be infective on inoculation into guinea-pigs. 

Chronic hemorrhagic peritonitis is a very rare form analogous 
to hemorrhagic pachymeningitis. The peritoneum in various parts, 
especially in the pelvis, is found covered with delicate layers of new- 
formed tissue containing many blood-vessels, and a hemorrhagic exudate 
may be present. 

Symptoms. — These are very vague and difficult to interpret. There 



DISEASES OF THE PERITONEUM 



147 



are usually indigestion and constipation and possibly some pain. As 
already indicated, in some cases there may be an abundant ascites, and 
the conditions under which chronic peritonitis may be suspected have 
been indicated. 

Treatment. — This is usually involved in the care of the associated 
cirrhosis or cardiac lesion. Otherwise it must be purely symptomatic. 

NEW GROWTHS OF THE PERITONEUM 

CANCER OF THE PERITONEUM 

Various new growths of the peritoneum have been described; of 
these cancer alone is frequent enough to be of clinical importance. Can- 
cer is rarely, if ever, primary in the peritoneum, but may be found 
secondarily to cancer in the abdominal organs, especially the uterus, 
stomach, or intestine. It occurs at the usual age and chiefly in women. 

The SYMPTOMS include the constitutional cachexia of cancer with 
abdominal pain, and the local signs of ascites. Fluid withdrawn may 
be bloody and may show cells with mitoses. After withdrawal of the 
fluid one or more masses may be felt in the abdomen. The condition is 
with difficulty distinguished from tuberculosis. Evidence of a primary 
growth in other parts, especially the uterus or stomach, must be sought. 

Ttreatment is purely palliative. 

ASCITES 
(Hydroperitoneum) 

Definition. — An accumulation of serous fluid in the peritoneal cavity. 

Etiology. — Ascites may be the result of local or general conditions. 
Local: (1) chronic disease of the peritoneum, simple, tubercular, or 
cancerous; (2) obstruction to the portal circulation, such as occurs in 
cirrhosis, cancer, or other disease of the liver, in thrombosis of the por- 
tal vein, in chronic congestion due to cardiac insufficiency of any kind, 
or to chronic pulmonary disease, especially emphysema or tuberculosis; 
(3) the growth of tumors in the abdomen which by pressure on 
lymphatics or blood-vessels may lead to ascites. General : ascites occurs 
as part of a general dropsy in heart disease. Bright 's disease, and in 
the final stages of severe anemia or cachexia, such as occurs in leukemia, 
cancer, and the like. The dropsy of heart disease is sometimes confined 
to the abdomen. 

Symptoms. — The girth of the abdomen gradually increases and 
the patient complains of weight or oppression. With large effusions the 
diaphragm is pushed upward, the lungs compressed and the patient 
suffers from dyspnea. Gastro-intestinal disturbances, loss of appetite 
and constipation are regularly present, and the urine is scanty. The 
associated symptoms are those due to the primary affection. 

Physical Signs. — Inspection: the abdomen is prominent, smooth, 



148 



DISEASES OF THE DIGESTIVE SYSTEM 



symmetrical. Usually the veins over it are dilated and sometimes vari- 
cose. If much stretched, the skin is shiny and perhaps shows stride. The 
umbilicus may bulge, especially in children. Palpation: the abdomen 
is tense or soft, depending upon the quantity of fluid present. A fluid 
wave may be obtained by placing the palm of one hand flat on one side 
of the abdomen and then lightly tapping the other side with the fingers 
of the other hand. To prevent confusion from the transmission of the 
impulse through the abdominal wall it is well to have a third person lay 
the ulnar border of one hand on the middle line of the abdomen and 
press gently downward, while the test is made. Percussion : the lower 
parts of the abdomen are dull, while the upper are tympanitic. Thus, 
the patient lying upon his back, the flanks are dull, the central parts, 
occupied by stomach and intestine, tympanitic. (See Fig. 23.) If the 




Fig. 23. — An ascitic abdomen: flatness below the line, tympany above. From the collection ot Dr. 

A. R. Lamb. 

patient stands or sits the dulness lies across the lower abdomen. If he 
turns on one side, the lower side becomes dull, the upper tympanitic. 
This shifting dulness is very characteristic. 

Diagnosis. — A distended bladder, large cysts, especially ovarian, 
and pregnancy with excessive amniotic fluid may be sources of error. 
None of the conditions named give the shifting dulness characteristic 
of ascites. The dulness is central, or unilateral, the flanks clear, and 
there is no material change with change of position. 

Character of Fluid. — This is usually clear serum, alkaline, of a 
specific gravity of 1.010 to 1.015, and containing a large amount of 
albumin. It may coagulate spontaneously. The fluid may be bloody, 
especially in tuberculosis or cancer, or chylous. The latter may arise 
from the ])resence of true chyle (very rarely) or from a fatty degenera- 
tion of cells present in the exudate. The study of the cellular content 



DISEASES OF THE- PERITONEUM 



149 



of the fluid is helpful. In simple ascites the cells are chiefly endothelial, 
in tuberculosis lymphocytes will predominate, in cancer mitotic nuclei 
may be found. 

Treatment. — The reduction of the fluid in the abdomen may be 
sought by reducing the intake of water and increasing the output by 
hydragogue cathartics and diuretics. Large doses of magnesium 
sulphate, or Epsom salts, or compound jalap powder may be given on 
rising. The effusion of digitalis or diuretin may be given for diuresis. 
Frequently these measures fail and tapping by trocar and canula must 
be resorted to and repeated as necessary. The puncture is regularly 
made in the mid-line midway between the umbilicus and the pubes. 
Care must always be taken to see that the bladder is first emptied. 



Ill 

DISEASES OF THE KIDNEYS 



ANOMALIES OF FORM AND POSITION 

Post-mortem observation has established the possibility of a large 
number of anomalies of the kidney. Those of clinical importance are: 
(1) Total absence of one kidney, a not very rare occurrence. The 
single kidney is usually considerably larger than normal. There may 
be a patent ureter on the side of the absent kidney. The rule is now 
established that before undertaking a nephrectomy the surgeon should 
make sure of the presence of a second organ. (2) Displacement of 
the kidney. Any part of the abdomen or pelvis may be occupied by 




Fig. 24. — Horse-shoe kidney. 



the displaced viscus. The kidne}^ may be fixed in the abnormal situation 
and may thus be mistaken for a tumor. (3) Double uretei*s may be 
found on one or both sides, a possibility of importance in cystoscopy. 
(4) Horse-shoe kidney. Not infrequently the lower poles of the two 
kidneys are fused, producing a form resembling a horse-shoe. This 
deformity is of importance from the possibility that the fused organ 
may bo mistaken for a tumor, or may cause difficulty in operations 
upon the organ, (See Fig. 24.) 
150 



ANOMALIES OF FORM AND POSITION 



151 



MOVABLE KIDNEY 
(Floating or Palpable Kidney. Nephroptosis) 

Definition. — An abnormal mobility of the kidney. Under ordinary 
conditions the kidneys are not palpable. If, on deep respiration, the 
lower pole of the kidney can be appreciated by the palpating fingers, 
the kidney is said to be palpable. If the fingers can be slipped over 
the upper pole, the kidney is movable. In some instances the kidney 
has what may be termed a mesonephron and can be displaced in any 
direction from its proper site, the floating kidney. 

Etiology. — In rare cases the condition is congenital. The acquired 
form is much more frequent in women, doubtless owing to the influence 
of tight-lacing and in some cases the relaxation produced by repeated 
pregnancies. Falls or heavy lifting may be the cause. Owing to its 
relation to the liver and consequent depression with every respiration 
the right kidney is much more frequently affected. The condition is 
often part of the general displacement of abdominal viscera, known as 
enteroptosis. 

Symptoms. — (1) There may be none. The condition is often dis- 
covered as an incident of the physical examination. (2) A feeling of 
dragging or weight in the right side of abdomen or in the back may be 
complained of. (3) Reflex symptoms of greater or less severity may 
be excited, (a) Nausea or vomiting, indigestion or constipation may 
be caused by a floating kidney. These symptoms are usually inter- 
mittent, and are increased by influences affecting the strain produced 
by the displaced organ, such as walking or hard work, (b) Dietl's 
crises. In some instances the patients suffer from intermittent attacks of 
sudden pain in the abdomen, with chill, fever, nausea and vomiting, 
as in renal or biliary colic. These attacks are attributed to kinking 
of the ureter, and are sometimes followed by the passage of unusual 
quantities of urine. Like attacks may also be induced by over-indulgence 
in food and drink. During the attacks the urine may contain blood, 
or albumin and casts, or urates in abundance. The kidney may be 
enlarged and tender to pressure, (c) Manifestations of neurasthenia 
or hysteria may be caused by the presence of a floating kidney. Such 
cases are rare. In most instances the movable kidney is an accidental 
accompaniment of the general condition. 

Diagnosis. — This must be based upon the identiflcation of the mass 
by its position, size, form and consistency. It must be remembered that 
the kidney may be met vnth in any part of the abdomen or pelvis. 

Treatment. — Many of the patients have no symptoms and require no 
treatment. Most of the cases with symptoms can be treated satisfactorily^ 
by an abdominal belt with a pad to support the kidney. Various corsets 
have also been invented for this purpose. Nephrorraphy may be re- 
quired in the more extreme cases, or where the simpler measure fails. 
Nephrectomy is contemplated only when all other measures fail, or the 
mobility is complicated by serious disease of the kidney. 



152 



DISEASES OF THE KIDNEYS 



CONGESTION OF THE KIDNEY 

Acute or Active Congestion. — An acute hyperemia of the kidney 
occurs in the early stages of acute nephritis. The etiology, pathologj-, 
symptoms, and treatment are those of acute Bright 's disease, and there 
is at present no advantage in attempting to separate the tAvo conditions. 

Chronic or passive congestion results (1) from disease of the heart 
or lungs resulting in failure of the return circulation in the inferior 
vena cava; (2) from compression of the renal veins by tumors, including 
the pregnant uterus, or ascitic fluid. The kidneys are large and firm, 
the capsule strips easily, the cortex is deeply congested and bleeds freely 
on section. The markings are exaggerated. Microscopically the veins 
are engorged, there is some increase of fibrous tissue, some sclerosis of 
the glomeruli and degeneration of the tubular epithelium, a chronic 
diffuse nephritis. The urine is scanty and of high specific gravity, 
contains a slight or moderate amount of albumin and casts, possibly 
blood. Otherwise the symptoms are those of the primary disease. 
Uremia is rare. 

Treatment must be directed to the cause. 

ANOMALIES OF THE URINARY SECRETION 

Anuria. — Suppression of the urine may result from (1) congenital 
absence of the kidneys. (2) Acute or chronic nephritis. No urine may 
be secreted for many hours. This occurs especially in severe acute 
infections, such as cholera, or yellow fever, and in the terminal stages 
of chronic nephritis. (3) Obstruction of both ureters by calculi, or 
of a single ureter, in case tlrere is only one, or the removal of an only 
kidney. (4) Collapse following severe operations. (5) The passing of 
a catheter. (6) Hysteria. 

Symptoms. — In some cases symptoms are long delayed. With com- 
plete anuria patients may live for one or two weeks. In other cases, 
especially in conditions producing acute nephritis, uremic symptoms 
appear early and the condition is quickly fatal. 

Treatment. — The obstructive cases require operation. In other 
cases, cupping or poultices over the loins, colonic irrigation ^^ith large 
quantities of hot salt solution, sweating by hot packs and pilocarpine 
given hypodermatically, and the free drinking of water may be 
effective. 

Hematuria. — Blood may appear in the urine from various causes. 
(1) General diseases: (a) Diseases associated with grave changes in 
the blood, pernicious anemia, leukemia, scurvy, purpura, malaria, and 
possibly other acute infections, (b) Diseases causing renal congestion, 
such as chronic endocarditis or myocarditis, or obstructive lesions of 
the lungs, such as interstitial pneumonia. (2) Local conditions: (a) 
Trauma of any part of the genito-urinary tract, (b) Acute or chronic 
nephritis, or infarction of the kidney, (c) Calculi in kidney, ureter, 
or bladder, (d) New growths of the kidney or bladder, (e) Tuber- 



ANOMALIES OF FORM AND POSITION 153 



culosis of the kidney or bladder, (f ) Acute inflammations of the pelvis 
of the kidney, bladder, or urethra, such as occur in pyelitis, cystitis, 
or urethritis. (3) Parasites, such as the Bilharzia hematobia. 

Diagnosis. — Blood in the urine tinges it dark red or black. It 
can be distinguished from hemoglobinuria only by the demonstration 
of the corpuscles under the microscope. 

Treatment must vary with the cause. Quiet is the one measure 
generally applicable. 

Hemoglobinuria. — Whenever rapid hemolysis takes place in the 
body, hemoglobin may be excreted unchanged in the urine. This may 
follow transfusion, the foreign blood being broken up. It may result 
from the action of certain poisons, such as potassium chlorate, arsen- 
urat€d hydrogen, or toluylendiamin. Infections such as malaria may 
be the cause, and hemolysis has also followed extensive burns or exhaust- 
ing exercise. 

Paroxysmal Hemoglobinuria is a clinical condition without definite 
pathology or etiology. Malaria and syphilis are adduced as causes. 
Often no cause can be found. Exposure to cold, or severe exertion may 
be the immediate cause of the attacks which characterize the affection. 
These attacks resemble the malarial paroxysm, beginning with a chill, 
followed by fever, amd sweating. In these attacks extensive hemolysis 
occurs from unknown causes. During or after the chill the patient 
passes blood-tinged urine and continues to do so for several days. He 
is then well for an indefinite period. The urine is either lightly or 
heavily colored by hemoglobin. The microscope shows no red blood 
cells. The urine regularly shows albumin derived from the blood. The 
presence of hemoglobin may be demonstrated by the spectroscope. The 
nature of the affection is unknown. It is supposed to be related to 
Raynaud's disease, symptoms of which sometimes appear with hemo- 
globinuria. 

Albuminuria. — The presence of albumin in the urine was first 
noted in Bright 's disease. For a long time its presence was regarded 
as indicative of nephritis. Accumulating evidence, particularly the 
use of the more delicate tests for albumin, has shown that it may be 
found in the urine of persons giving no evidence of Bright 's disease 
or any other renal lesion. It may appear in the urine of persons 
apparently in perfect health, but it is generally agreed that albumin 
is not excreted by an entirely normal kidney. Practically, we know 
that some persons can go on for years excreting albumin in small 
quantities either constantly or intermittently without developing other 
signs of nephritis, or other renal lesion. We therefore classify the 
condition as 

1. Albuminuria without gross renal lesions, including (a) Physio- 
logical albuminuria, in which albumin appears transiently or constantly 
in the urine of apparently healthy persons. Various conditions may 
lead to the excretion of albumin, such as the ingestion of large amounts 
of albuminous foods, especially eggs, severe exertion, or cold bathing. 



154 



DISEASES OF THE KIDNEYS 



In other persons no cause can be assigned. The condition has been 
termed cyclic, paroxysmal, intermittent, or orthostatic albuminuria, as 
the individual case suggested, (b) Hemic albuminuria. Grave anemia 
from any cause may lead to mild albuminuria, (c) Febrile albuminuria. 
Fever of any kind may cause the presence of albumin in the 
urine. In fever the urine is regularly scanty, of high specific gravity, 
contains a trace of albumin, and often hyaline and granular casts. 
With the subsidence of the fever the urine becomes normal again. A 
large percentage of all fever cases show these changes. They are 
attributed to the action of toxins. In some cases there are doubtless 
organic changes, such as the cloudy swelling seen post-mortem in fatal 
cases. In other cases it is possible that the kidneys remain normal, 
(d) Nervous albuminuria. After epileptic seizures, in apoplexy, tetanus, 
exophthalmic goitre, or after injuries to the brain, albumin may appear 
in the urine. 

2. Albumin with definite kidney lesions. (a) Congestion, acute 
or chronic, of the kidney, (b) Nephritis, acute or chronic, of any 
type, (c) Suppurative inflammation of any part of the urinary tract, 
(d) Tumors of the kidney, ureter, or bladder. The significance of 
the presence of albumin in the urine will be determined by the con- 
clusion as to its cause. It is usually a symptom of importance, but 
in some cases exists for years without apparent harm. 

Pyuria. — Pus in the urine may come from (1) Suppurative inflam- 
mation in the genito-urinary tract; (a) urethritis, most often gonor- 
rheal; (b) cystitis or prostatitis; (c) pyelitis; (d) pyelonephritis. 
(2) Abscesses or suppuration in other parts discharging in the urine; 
(a) leucorrhea; (b) pelvic, perinephritic, or appendical abscesses. 

Pus must be identified by the microscope. With pyuria the urine 
is often alkaline, but may remain acid. 

Chyluria. — The urine may present a milky appearance from ad- 
mixture with chyle. The condition may arise from infection with 
filaria, or in some cases by chance commimication of lymphatic vessels 
with the pelvis of the kidney or ureter. Chylous urine is frequently 
pink from the presence of blood. Under the microscope the fat globules 
and possibly red blood cells are seen. 

Lithuria. — The excretion of excessive amounts of uric acid and 
urates is thus designated. Both these substances are end results in the 
metabolism of nitrogenous foods, being derived from the nucleo-proteids. 
Their elaboration in the body runs parallel with the formation of urea, 
but is not identical with the latter. Uric acid may be derived either 
from the nucleo-proteids of the food, or those of the body itself, and 
is thus distingTiished as exogenous or endogenous. The amount excreted 
must therefore depend in part upon the diet, in part upon the breaking 
down of body cells. We have ordinarily no means of determining how 
much of the uric acid appearing in the urine is derived from each of 
these sources. The problem of interpreting variations in the excretion 
of uric acid is therefore so complex that we can at present make prac- 



ANOMALIES OF FORM AND POSITION 



155 



tically no deductions of clinical value from observations of the excretion 
in individual cases. Exhaustive studies of the metabolism of gout have 
failed to demonstrate any constant excess or deficiency of the uric 
acid of the urine. At most we have learned that just before an attack 
the excretion of uric acid is diminished, while as the attack subsides 
it is increased. The diagnosis of gout cannot be made from the study 
of the urinary conditions alone. 

Deposition of uric acid and urates in the urine is a common occur- 
rence, the sediment having a pale amorphous appearance if the urates 
are in excess, or appearing as minute reddish crystals, the "brick-dust" 
sediment, if uric acid crystals are present in quantity. Such precipita- 
tion of urates and uric acids results from changes in the temperature, 
specific gravity, reaction and content of other substances, especially the 
chromogen of the urine. Such deposits do not, therefore, necessarily 
mean increased elimination. 

In brief, excretion of uric acid and urates will depend chiefly upon 
the amounts ingested and the body metaboUsm. Sedimentation of uric 
acid and urates will depend in part on the presence of excessive amounts, 
but more largely upon the other characters of the urine. It is a 
common phenomenon in all febrile cases. Recognition of these facts 
should prevent us from attaching too great value to the appearance of 
sediments containing uric acid, or to estimations of the amount to be 
found in the urine of any individual patient. 

Oxaluria. — The deposition in the urine of crj^stals of calcium 
oxalate is of importance because of the frequency with which this sub- 
stance forms concretions in the kidney or bladder. Calcium oxalate 
may be derived from food or result from the metabolic activities of 
the body. The exact origin of the endogenous portion is not known, 
and therefore the significance of an increased output, apart from the 
question of intake, is still undetermined. The effort to lessen the output 
must be directed to the removal from the diet of the substances richest 
in this salt, such as rhubarb, spinach, and tea. 

Cystinuria is a very rare condition in which the colorless hexagonal 
crystals of cystin appear in quantity in the urine. They may be the 
basis of calculi. Excessive excretion belongs to certain individuals and 
often persists throughout life. The disposition may be hereditary. 
The cystin results from a defective metabolism of protein. 

Phosphaturia. — Phosphates are normally present in the urine. They 
may be deposited by reason of excessive excretion, or, when normal in 
quantity, because of a change of the normally acid urine to an alkaline 
reaction. Only to the former condition should the term phosphaturia 
be applied. True phosphaturia is often associated with neurasthenia 
or disturbances of the sexual organs. The phosphates excreted are 
mainly those of sodium, potassium, calcium, and ma^Tiesium. Of these 
the sodium and potassium salts are the more easily soluble. By reason 
of this fact an excessive excretion of Ca and Mg is sometimes the 
explanation of a phosphaturia, these bases uniting with phosphoric 



156 



DISEASES OF THE KIDNEYS 



acid to form the less soluble salts and also diminishing the amounts 
of sodium and potassium phosphates upon which the acidity of the 
urine depends. 

Indicanuria. — The intestinal bacteria break up the proteids of the 
food and produce indoL The indol is taken into the circulation and 
oxidized, probably in the liver, into indoxyl, which combines mth sul- 
phuric acid to form the so-called ethereal or conjugate sulphates. This 
indoxyl when treated with strong oxidizing agents is broken up with 
the formation of indican or indigo. The common test for indican con- 
sists in adding to 5 to 10 c.c. of the urine an equal amount of Ober- 
meyer's reagent, composed of strong hydrochloric acid (specific gravity 
1019) containing two parts per thousand of ferric chloride. One to 
two c.c. of chloroform is then added and the w^hole gently mixed by 
repeated inversion of the tube. If indican is present, it will be taken 
up by the chloroform, which on allowing the mixture to settle sinks to 
the bottom and appears stained more or less deeply blue. A trace of 
ij.dican may be present in health. In large amounts it is abnormal. 
It is most abundant in cases where intestinal fermentation is most 
active, such as typhoid fever, intestinal obstruction, and the like. Its 
presence has most value in the milder functional intestinal disorders, 
often described as "biliousness," where the occurrence of excessive 
indican formation suggests the desirability of reducing the proteid 
intake and of instituting measures for the lessening of intestinal 
fermentation. 

UREMIA 

Definition. — Uremia is the condition of intoxication developed in 
acute or chronic nephritis. The cause is unkno"WTi. (1) It was long 
attributed to the retention of substances normally excreted. Urea, the 
potassium salts, creatin, and uric acid have been successively named 
as the harmful substances, but proof of their relation to the intoxication 
has never been given. (2) An internal secretion, like that of the 
thyroid, has been assumed to explain the phenomena, but this remains 
a pure hypothesis without evidence to support "it. (3) Still another 
theory attributes the symptoms to the effects of neurolysins produced 
in the diseased kidneys upon the nerve centers. The fact remains that 
at present there is no satisfactory^ explanation of the condition known 
as uremia. The greatest difficulty in the understanding of the matter 
arises from the fact that the phenomena of uremia are not those of 
anuria, and that patients have been known to survive periods of anuria 
of two weeks, or in one ease nineteen days. 

Symptoms. — These are developed either swiftly or slowly. In some 
cases, especially in acute nephritis, the symptoms come so swiftly that 
the cases are properly termed fulminant, in other eases the phenomena 
of uremia are gradually developed in the course of years. Commonly, 
cases are classified as acute or chronic, according to their rapidity of 
evolution. (1) Headache is a frequent and often an early symptom. 



ANOMALIES OF FORM AND POSITION 



157 



It is usually occipital, and may be either mild or agonizing. (2) Ocular 
symptoms are common. Impairment of vision may result from optic 
neuritis, but apart from demonstrable changes in the retina, vision 
becomes dim or total blindness supervenes. (3) Dyspnea is frequent 
and severe, and may be constant or paroxysmal. It is regularly worse 
at night, and orthopnea is not uncommon. In the severe types Cheyne- 
Stokes respiration is often seen. (4) Nausea., vomiting, and diarrhea 
are common and sometimes the only symptoms. The vomiting may be 
only occasional, sometimes it is persistent. Diarrhea, once it appears, 
is likely to be persistent and intractable. In some cases marked organic 
lesions, such as membranous colitis, are found post-mortem, but in 
others the intestines appear normal. (5) Muscular twitchings are 
usually present. They involve the muscles of the face or other part, 
or the whole body. (6) Delirium, coma, or convulsions develop in 
the severer, cases. The delirium may be mild, wandering, or maniacal 
in type. The coma is usually profound with complete insensibility and 
loss of control of the sphincters. The pupils during coma may be 
normal, or contracted, or even dilated. Contraction is the more frequent. 
The convulsions are epileptic in type and may be either local or general. 
Once developed they are usually repeated at short intervals, the patient 
remaining comatose between them. Monoplegia or hemiplegia may 
develop during or after a convulsion and may persist for some time, 
but such paralyses regularly clear up in those who survive. (7) The 
urinary symptoms are not constant. The urine usually shows on ex- 
amination the characters belonging to a parenchymatous or interstitial 
nephritis. 

'Diagnosis. — The recognition of milder degrees of uremia often 
depends upon the thorough investigation of patients complaining of 
minor ailments such as headache, neuralgic pains, insomnia, occasional 
nausea or vomiting. Careful examination of the patient may develop 
the characteristic conditions of a chronic nephritis, the findings being 
confirmed by the urinalysis. Routine examination of the urine, both 
chemically and microscopically, in all patients, more especially those 
over forty, is the only safe-guard against error. Uremic coma in a 
patient seen for the first time is difficult of diagnosis. It is most 
likely to be confounded with coma due to alcoholism, cerebral hemor- 
rhage, opium-poisoning, or diabetes. In uremic coma th-e unconscious- 
ness is profound, the pupils are equal, either dilated, normal or con- 
tracted, there is no deviation of the eyes. The breath has a peculiar 
urinous odor. Usually there is no paralysis, but a monoplegia or 
hemiplegia may be present, which cannot at the moment be dis- 
tinguished from paralysis due to cerebral hemorrhage. If the patient 
survives, the paralysis gradually disappears. Lumbar puncture gives 
normal cerebrospinal fluid, usually under increased pressure. The 
urine, withdrawn by catheter, contains albumin, usually in consider- 
able quantity and abundance of casts. The specific gravity may be 
high or low. There may be definite suggestions of nephritis in thickened 



158 



DISEASES OF THE KIDNEYS 



arteries, increased blood pressure and hypertrophy of heart or in the 
presence of edema and anemia. 

Alcoholic coma is less profound. The patient can usually be roused, 
either by pressure over the supra-orbital nerves, or by the policeman's 
more crude, but satisfactory method of beating the soles of the shoes 
with his stick. The face is flushed, the breath heavy with the odor 
of alcohol, the pulse rapid and bounding, with no change in the pupils, 
no paralyses. The possibility that alcohol may have been given to a 
patient suffering from another cause must be remembered. 

Opium-poisoning is marked unmistakably by the profound coma, 
pin-point pupils, and slow respiration, the rate falling to 12 or 8 or 
less in the minute. 

Diabetic coma usually occurs in persons who are emaciated by 
their disease ; the breath has an ethereal odor, ascribed to acetone ; the 
skin is dry and harsh ; the urine is of high specific gravity and contains 
sugar. 

In protracted cases uremic conm has been confused with the stupor 
of typhoid fever, cerebrospinal fever, or tubercular meningitis. 

The TREATMENT of Uremia is included in that of chronic nephritis. 

FUNCTIONAL EFFICIENCY OF THE KIDNEYS 

In studying the effects of nephritis we much concern ourselves not 
only with the presence of abnormal elements such as albumin and casts 
in the urine, but with the problem of the influence of disease upon the 
functions of the kidneys as the chief excretory organs of the body. For 
many years the specific gravity of the urine and the total quantity for 
24 hours furnished the only standard for such judgments. The nor- 
mal quantity of urine for 24 hours is 40 or 50 ounces, the normal specific 
gravity from 1015 to 1025. As the quantity increases the specific gravity 
normally falls. The rough rule has been established that the product 
of the last two figures of the specific gravity by 2 or 2.33 (Haser's fac- 
tor) gave the solid excretion in grams, and if this exceeded 35, the 
urinary excretion could be regarded as satisfactory. Many influences, 
such as the diet and fluid intake, exercise, the activity of the skin and 
bowels, modify the factors in this method of computation and affect the 
result. The rule expresses only the minimum standard of efficient ex- 
cretion and must be loosely applied in any individual case. 

Efforts have been constantly made to obtain a more exact standard. 
This was sought in the determination of the percentage and daily out- 
put of urea, because of the assumed relationship of the retention of 
urea to the symptoms of uremia. The information thus obtained has 
not proven of practical value, and the effort to judge of the efficiency 
of the kidneys by computation along this line has been abandoned. 

More recently estimation of the freezing-point of the urine after 
the method of Koranyi, or calculation of the electrical conductivity of 
the urine, has been proposed as a standard of renal efficiency, but after 



FUNCTIONAL EFFICIENCY OF THE KIDNEYS 



159 



protracted trial these procedures have been found no more satisfactory 
and are no longer employed. 

At the present time the attention of students of this subject is 
directed not to the estimation of the total excretory activity of the kid- 
neys so much as to their ability to excrete individual substances, and 
more especially sodium chloride and water. 

Chloride Excretion. — It has been clearly shown that diseased kid- 
neys vary greatly in their ability to excrete sodium chloride. The 
normal chloride excretion varies between 10 and 15 grams per day. In 
certain cases of nephritis the total may fall to 1 gram or even less. In 
such cases under ordinary conditions there results a marked retention 
of sodium chloride in the blood and the tissues of the body. Upon such 
salt retention edema in some cases depends, and the amount of edema 
is found to vary with the retention or excretion of the chlorides. The 
value of a salt-poor or relatively salt-free diet in these conditions has 
been established and restriction of the salt intake is now recognized 
as a potent therapeutic measure not only in nephritis but in other con- 
ditions marked by serous effusions. 

The study of the chloride intake and output in connection with the 
water intake and output and the weight of the patient has therefore been 
established as a measure of value both in the diagnosis and prognosis of 
nephritic lesions. 

If the kidney still retains the ability to excrete salt normally or nearly 
so, the reduction of nephritic edema may easily be brought about by 
the employment of a diet having a low salt value. 

Therein lies in part at least the explanation of the efficacy of a milk 
diet in nephritis. If, on the other hand, the ability to excrete salt is 
impaired or nearly lost the problem of reducing nephritic edema is much 
less easily solved. 

Experimental evidence indicates that salt excretion is most reduced 
in processes involving the epithelium of the tubules, while vascular 
lesions affect it slightly or not at all. Salt retention should, therefore, 
be characteristic of nephritis affecting especially the epithelium (paren- 
chymatous nephritis), while it should be less marked in those types of 
nephritis involving especially the glomeruli and sparing the tubules 
(interstitial nephritis). But we are not yet in a position to apply these 
propositions as criteria to determine the anatomical type of nephritis 
with which we may be dealing. 

Water Excretion. — In like manner in certain cases of nephritis the 
power to excrete water seems to be impaired or preserved, independently 
of the chlorides. For this reason the free administration of water may 
be beneficial in some cases of nephritis and harmful in others. Impair- 
ment of ability to excrete water indicates lesions particularly affecting 
the glomeruli, but in certain cases of nephritis in which the glomeruli 
are extensively damaged the function of water excretion seems to be 
taken over by the epithelium of the tubules and carried on so actively 
that even an excess of water may be excreted (interstitial nephritis). 



160 



DISEASES OF THE KIDNEYS 



The study of the influence of the free administration of water or its 
restriction upon the urinary secretion, the edema, and the weight of 
the patient is of great value in determining the proper procedure. The 
normal kidney will excrete water freely up to 100 or 120 ounces in 24 
hours, and the higher the amount, as a rule, the larger the proportion 
of the water excreted under ordinary conditions by the kidney. If the 
kidney be seriously diseased, the power of excreting water may be 
notably impaired, and no diuresis follow the addition of 50 or 60 
ounces of water to the fluid intake. It is not uncommon to find the 
total water excretion of the kidneys limited to 10 ounces or less per 
day. Under such conditions the free administration of water may be 
harmful, and the other avenues of eliminating fluid must be resorted to. 
On the other hand, if the water excretion is still free it may be advan- 
tageous to give large amounts. 

Excretion of Other Substances. — Efforts to test the functional capa- 
city of the kidneys by the administration of methylene blue, salicylic acid, 
or potassium iodide by mouth, or phenolsulphonephthalein hypoder- 
matically have been made, but the value of these methods in calculating 
the efficiency of the kidneys has not yet been established. They have, 
however, been employed successfully in comparing the relative efficiency 
of the two kidneys in cases in which one only is impaired. 

ACUTE NEPHRITIS 
(Acute Blight's Disease) 

Definition. — An acute inflammation of the kidney, involving to some 
extent both the interstitial and parenchymatous tissue. 

Etiology. — Acute nephritis occurs at all ages, but especially in 
childhood. (1) It may arise without apparent cause, a primary nephritis. 
It is more often due to the following influences: (2) Exposure to cold 
or wet. (3) The poisons of the acute infectious diseases, especially 
scarlet fever. (4) Alcoholic excesses predispose to the disease. (5) 
Pregnancy. The nephritis complicating pregnancy is best classified as 
an acute nephritis, though presenting many points peculiar to itself. 

Morbid Anatomy. — The gross appearances are not constant. The 
kidneys are usually somewhat enlarged, softer than normal, the capsule 
free, the surface smooth and either congested or pale, the section cloudy, 
the markings being less distinct than noiTQal. Microscopically the 
lesions of acute nephritis are of very irregular distribution and in 
different eases affect different parts of the tissue, the glomeruli, the 
tubules, the interstitial tissue especially. Thus glomerular, tubular, and 
interstitial types of acute nephritis have been described by different 
authors, depending upon the part found most affected. It is, however, 
impossible to distinguish these groups clinically. The lesions found 
in the kidney tissue may be grouped under the heading's of congestion, 
degeneration, exudation. The congestion varies greatly in degree and 



FUxNCTIONAL EFFICIENCY OF THE KIDNEYS 161 



in distribution. It may be absent entirely. Degenerative changes are 
always present, especially in the epithelium of the tubules. Different 
parts of the tubules are variously affected, the convoluted tubes usually 
showing the most marked lesion. The epithelium becomes granular or 
fatty, or may break down completely, and the nuclei may disappear. 
The glomeruli show similar changes. An exudation of serum, fibrin, 
and leukocytes or red cells may be found sometimes in the tubules, 
sometimes in the glomeruli, sometimes in the interstitial tissue, rarely 
in all parts of the kidney in any one case. The amount of such inflam- 
matory exudate varies greatly. In some it is so slight as to be seen 
with difficulty. In other cases it is abundant, the tubules, glomeruli, 
and even the interstitial tissue showing leukocytes and other inflam- 
matory products. Councilman has described a special variety of acute 
nephritis in children in which the exudate in the kidney consists almost 
wholly of plasma cells. 

Symptoms. — The onset is either (1) abrupt or (2) insidious. (1) In 
the abrupt cases the invasion is marked by malaise, fever, headache, 
possibly nausea and vomiting, and some edema of the face and ex- 
tremities, and possibly the abdomen and chest. (2) In the insidious 
cases the invasion is very gradual, marked by a little malaise, lassitude, 
and pallor. On examination of the urine in either case the characteristic 
changes are found. The urine is scanty in amount, high colored, pos- 
sibly bloody, of high specific gravity, w4th albumin in abundance and 
microscopically many casts, hyaline, granular, epithelial and sometimes 
blood-casts, often red and white blood cells and much granular detritus. 
There may be complete suppression of the urine for many hours, 
possibly 1 or 2 days. Once the disease is established the course varies. 
(1) Some patients recover w^ithin a week or two. (2) Others develop 
severe uremic symptoms, headache, dyspnea, delirium, coma, possibly 
convulsions, and die within a few days. (3) The majority of the 
cases run a protracted course, the symptoms already enumerated vary- 
ing from time to time, until ultimately they recover, or the condition 
of chronic nephritis is developed, usually of the parenchymatous, but 
sometimes of the interstitial type. In these cases the marked s^nnptoms 
are (1) edema of the dependent parts, especially the legs and scrotum, 
often a general anasarca involving the pleura and peritoneum. The 
anasarca may be very persistent. (2) Anemia is always marked. (3) 
Loss of appetite, nausea, and occasional vomiting. (4) Variable uremic 
symptoms, headache especially. (5) Dyspnea is absent, except on 
exertion or when the chest is full of fluid. (6) The urine remains 
scanty and of high specific gravity, Avith albumin and casts, but the 
albumin gradually lessens and the casts likewise. Blood usually disap- 
pears after the acute stages. (7) In many cases the pulse tension is 
high, the arteries gradually thicken, the heart hypertrophies, and the 
vascular conditions characteristic of chronic nephritis develop. 

Diagnosis. — This rests on the combination of symptoms and urinarv^ 
findings. The chief source of confusion is the febrile albuminuria. In 
11 



162 



DISEASES OF THE KIDNEYS 



any febrile disease the urine may show a trace of albumin, with hyaline 
and granular casts. As the fever subsides these disappear. Such cases 
should not be classed as acute nephritis. 

Treatment. — The essential point is as complete rest for the kidney 
as possible. This is secured by (1) rest in bed; (2) a fluid diet, 
especially milk or the low-salt diet (p. 593), is indicated; (3) free 
purgation by salts; (4) hot packs or hot air baths to secure free sweat- 
ing daily or every other day. Pilocarpine may be given for the same 
purpose, gr. 1/12-1/10 for an adult. (5) Water should be given 
freely as a diuretic if freely excreted. The anasarca sometimes re- 
quires further interference. Effusions in the peritoneum or pleura 
should be withdrawn when large enough to embarrass respiration by 
pressure. They usually return promptly. The legs and scrotum may 
be punctured with a needle or Southey's tubes may be employed, but 
much the best plan is to make several long incisions, under cocaine, 
through the skin. All wounds must be treated aseptically. For anuria, 
poultices may be applied over the loins, and rectal irrigations of normal 
salt solution heated to 105° to 110° F. Purgatives and sweating may 
be employed. For severe uremic symptoms venesection is indicated 
if the pulse tension is high. Nitroglycerine may be given instead. 
Chloral alone or chloral and sodium bromide may be given by the 
mouth or rectum. Morphine may be employed hypodermatic ally to 
prevent or mitigate convulsions. Chloroform may be used for the same 
purpose. Lumbar puncture has been employed for the reduction of 
intracranial pressure, apparently with good results. While these 
palliative measures are being employed, every effort must be made to 
promote diuresis and lessen the work of the kidney by the measures 
already suggested. As the condition progresses the diet must be 
enlarged by the addition of cereals, fruits, and vegetables. The anemia 
should be treated by iron, and the treatment gradually modified to that 
of a chronic nephritis. 

CHRONIC NEPHRITIS 

The pathological anatomy and the clinical history of cases of 
chronic nephritis vary greatly in different patients. Numerous classifica- 
tions, all more or less unsatisfactory, have been made and cast aside. 
We have come to accept two fairly definite types, the parencManatous 
and interstitial, named from the predominant feature of the pathological 
change in each, although it is recognized that, strictly speaking, the 
terms are misleading, for in every chronic nephritis all parts of the 
kidney, tubules, glomeruli, interstitial tissue, are involved to some 
extent. We also know well that many cases fall neither in one gi^oup 
nor the other, but present a mixed and unclassifiable picture. Never- 
theless these two fairly well differentiated types at pr'esent serve as 
the most satisfactory categories under which to describe the phenomena 
of chronic nephritis. 



FUNCTIONAL EFFICIENCY OF THE KIDNEYS 



163 



CHRONIC PARENCHYMATOUS NEPHRITIS 
(Large White Kidney) 

Definition. — A chronic inflammation of the kidney affecting especially 
the parenchyma of the organ. 

Etiology. — (1) It is often the sequel of an acute nephritis. (2) The 
excessive use of alcohol, syphilis or tuberculosis predisposes to it. 
(3) In the great majority of cases the disease appears without recog- 
nizable cause. 

Morbid Anatomy. — Many varieties of chronic parenchymatous 
nephritis are described, such as the large white kidney of Wilks, the 
large red, and the small white. Neither the size nor the color of the 
kidney is of great importance, but these three types may be taken as 
representing the variations commonly seen. The large white kidney 
described by Wilks is much larger than normal, the two organs some- 
times weighing as much as 25-30 ounces (800-900 gms.). (See Fig. 25.) 
They are firm, the capsule is free or but slightly adherent, the surface is 
pale gray or slightly yellow, the cortex is thick, the markings are much 
obscured. Microscopically the lesions are found irregularly distributed. 
There is a moderate increase of connective tissue, which in places shows 
foci of round-cell infiltration. The striking changes are in the tubules 
and glomeruli. In the tubules there is marked degeneration of the 
epithelium, often with desquamation. The lumen of the tubes often 
shows casts. The convoluted tubules are most affected. The glomeruli 
are variously changed, some larger, others smaller, some completely 
atrophic. In general, Bowman's capsule is thickened and its epithelial 
covering sometimes increased. Over the tufts there is an increase of 
cells. Many of the tufts sliow hyaline degeneration, and some are 
converted into fibrous tissue. The walls of the blood-vessels, especially 
the smaller, may show thickening. 

The large red kidney presents no material difference except in color. 
The small white kidney is regarded as a late stage of the large white, 
in which there has been a marked increase of connective tissue with 
subsequent contraction, reducing the size of the kidney. These kidneys 
are smaller than normal, firmer, the capsule is more adherent, the 
surface is pale, the cortex of normal width or less, the markings in- 
distinct. Microscopically the lesions have the same character as in 
the large white kidney, except that there is more fibrosis, both in the 
interstitial tissue and the glomeruli. 

Associated Lesions. — In fatal cases fluid is found in the serous 
cavities, especially the pleura and peritoneum. There may be an acute 
pleurisy, pericarditis, or peritonitis, representing a terminal com- 
plication. 

Symptoms. — (1) AVhen the disease is a sequel of an acute nephritis, 
anemia, edema, dyspnea, and the urinary conditions persist. (2) In 
other cases the invasion is insidious, (a) Anemia develops early, 
(b) Gastric symptoms are usually marked; loss of appetite, possibly 



164 



DISEASES OF THE KIDNEYS 



nausea and vomiting. The bowels are constipated, (c) Edema appears, 
in the anldes first, or in the face, later fluid is found in the peritoneum, 
pleura, or pericardium, (d) The urine shows a reduced quantity, of 
high specific gravity, containing large quantities of albumin and many 
casts. Blood cells may appear in the urine, but are not so frequent 
as in the acute form, (e) Drowsiness and headache are common, but 




Fig. 25. — The large white kidney: cortex of normal thickness and its markings fairly preserved. 

the severer uremic manifestations, such as muscular twitchings, delinum, 
coma, and convulsions, are comparatively infrequent, (f) The heart 
may hypertrophy and the vessels show sclerosis, but these changes are 
more common in the interstitial nephritis. They are therefore apt 
to be associated with the small white kidney rather than the larger 
forms. 

Course and Prognosis. — Once the disease is well established it is 



FUNCTIONAL EFFICIENCY OF THE KIDNEYS 



165 



rarely cured. It runs a chronic course and the patients, after months 
or years, succumb either to the general anasarca and edema of the 
lungs^ or to a complicating inflammation of one of the serous mem- 
branes, or to uremic convulsions. During the course of chronic 
parenchymatous nephritis exacerbations closely resembling acute 
nephritis are frequent. 

Treatment.— The main lines of treatment are those of acute nephritis. 
The patient must lead a quiet life ; if edema is present he had best 
be kept in bed or in a chair. Milk should form the basis of the diet, 
with the addition of cream, cereals, and syrup, as in Von Noorden's 
diet. Water should be given according to the ability of the kidney to 
excrete it. Diuretics, the acetates of potassium and sodium, diuretin 
and the like, may be tried at times, but the results are usually disap- 
pointing. Anemia is treated by the administration of iron. Basham's 
mixture is usually chosen. The bowels must be kept open and the skin 
active. When possible, life in a mild, uniform climate, such as that of 
Southern California, is desirable. Anasarca must be treated as in 
acute nephritis. When all other methods fail, decapsulation of the 
kidneys may afford relief and indefinitely prolong the patient's life. 

CHRONIC INTERSTITIAL NEPHRITIS 

(Granular or Contracted Kidney) 

Definition. — A chronic nephritis involving especially the interstitial 
tissue. 

Etiology. — Three forms of contracted kidney are recognized. (1) A 
secondary form which follows or develops from a chronic parenchyma- 
tous nephritis. In this type the etiology of chronic parenchymatous 
nephritis applies. (2) The arteriosclerotic Iddney, in which the. disease 
is part of a general arteriosclerosis, and is due to the causes producing 
the latter. (3) A primary type, often developing without definite cause. 
A number of factors are believed to influence the production of such 
nephritis: (a) the excessive use of alcohol; (b) faulty digestion or 
metabolism due to overeating; (c) gout or diabetes; (d) acute in- 
fectious diseases, especially scarlet fever, are sometimes followed by 
contracted kidney. The disease is common in people over 40 years 
of age, but is seen occasionally in earlier years, even in childhood. 

Morbid Anatomy. — The kidneys are small, the two sometimes 
weighing only 50-60 grammes; they are hard; the capsiile is tightly 
adherent, so that in stripping it off, bits of the cortex are torn away 
(see Fig. 26) ; the color is usually red; the surfaces very coarsely 
granular, and often marked by numerous small cysts, caused by 
obstruction of some of the tubules or glomeruli; the substance cuts 
with resistance; the cortex is thin, in places almost obliterated; the 
markings very indistinct (see Fig. 27). Microscopically the striking 
feature is the marked increase of connective tissue everywhere. In 
the dense strands of fibrous tissue the glomeruli and tubules appear 



166 



DISEASES OF THE KIDNEYS 



to be strangled. Some few are normal, most of them show pronounced 
changes. Many of the glomeruli are represented only by fibrous patches, 
many are very small with the capsule much thickened, the epithelium 
lining the capsule and covering the tuft much increased. Some few 
glomeruli appear distended (from obstruction). Similarly many of the 
tubules are obliterated, many are very small, some few are distended. 
The epithelium shows degenerative changes, but not so markedly as in the 
parenchymatous type, and is often simply flattened. Many of the cells 
are broken down or desquamated. The lumina of the tubes is often 
filled by casts. The blood-vessels are notably thickened, especially their 
middle coats. It must be understood that the description here given is 
that of the typical example. In many cases the chang^es are less marked 
and so closely resemble those of chronic parenchjanatous nephritis that 



Fig. 26. — Small contracted kidney, showing the rough, granular surface, and at the upper pole 
a small cyst. 

Fig. 27. — Section of the contracted kidney, showing the atrophic cortex with obliterated mark- 
ings and cysts, and the fatty tissue about the pelvis. 



it is impossible to say from the anatomical conditions alone in which 
class a given kidney belongs. Also, there are cases of chronic nephritis 
which with all the data known (history, urinalysis, gross and micro- 
scopic examination of the kidney) cannot be satisfactorily grouped 
under either of the classes here given, but must be designated simply 
as chronic nephritis. 

Associated Lesions. — The heart is hypertrophied, the aorta may 
show atheroma, and the smaller vessels are thickened. The lesions of 
cerebral apoplexy, a frequent cause of death, may be found. Dropsical 
effusions may be present. Acute pleurisy, pericarditis, or peritonitis 
is occasionally seen. 

Symptoms. — The invasion of the disease is so insidious that it is 
often not discovered till far advanced, or till some of the complications 



Fig. 26. 



Fig. 27. 



r 




FUNCTIONAL EFFICIENCY OF THE KIDNEYS 167 



bring about a careful examination; not infrequently the condition is 
discovered only at autopsy. The patient most often complains simply 
of not feeling well, or of headache, or insomnia, or dyspnea, or dis- 
turbance of digestion with loss of appetite and flatulence, or of polyuria. 
Examination then discloses: (1) Urinary condition. The urine is in- 
creased in quantity, 2000-4000 c.c. in 2-i hours, the specific gravity is 
1010-1015, a trace of albumin is present, and hyaline and granular 
casts. The solid constituents are diminished in proportion and their 
total daily elimination is low. 

(2) The heart is hypertrophied, especially the left ventricle, the 
second aortic sound is exaggerated, the pulse tension is increased, some- 
times enormously. The sphygmomanometer readings vary from 175 
to 300 mm. of Hg. The arteries are thickened and more or less rigid. 

(3) The retina may show a diffuse retinitis or scattered patches 
of hemorrhage and atrophy. The eye changes belong, as a rule, to the 
later stages. 

(4) Edema or anasarca is rarely found until the heart fails under 
the increased peripheral pressure and congestion results. 

Once the disease is established, the course is protracted and variable, 
(a) The patient may go on for many years with health slightly impaired, 
but suffering very little, life being ended by some intercurrent acute 
disease, especially pneumonia, (b) Severe uremic symptoms, headache, 
delirium, coma, or convulsions may be fatal at any period. Not infre- 
quently the advent of coma or convulsions is the first sign of the disease 
to attract attention. Vision may be impaired or blindness result from 
the retinal changes, (c) Dilatation and failure of the heart with con- 
gestion and edema often mark the close of the disease, (d) Apoplectic 
attacks are frequent. A single attack may be fatal, or there may be a 
number. In some cases a transient monoplegia or hemiplegia occurs. 
Localized edema of the brain or spasm of the cerebral arteries has been 
suggested as the explanation of such temporary loss of power. 

The BLOOD regularly shows a secondarj^ anemia of moderate grade. 

Diagnosis. — This must be based upon the presence of the urinary 
changes with the characteristic changes in the heart and arteries. The 
examination of the retinas may be important. The possibility of latent 
interstitial nephritis makes necessary the examination of the urine in 
all patients, more especially those over forty years of age. 

Prognosis. — Chronic interstitial nephritis may exist for many years 
without serious results. On the other hand, the disease is incurable. 
The changes in the heart and vessels are, as a rule, most important 
elements in the prognosis. The estimation of the blood pressure is 
helpful. Marked changes in the retina are signals of danger; with 
them patients rarely survive more than a year. 

Treatment. — Except in the emergencies caused by sudden heart 
failure, or uremic crises, the treatment of chronic interstitial nephritis 
consists mainly in the regulation of the diet and life of the patient, 
(1) The diet should be of mixed composition and abundant enough 



168 



DISEASES OF THE KIDNEYS 



to maintain the nutrition of the patient. It should be determined by 
the appetite of the patient and his ability to digest rather than by 
theories as to what is indicated by the disease. Moderation is necessary. 
Alcohol in any form is withdrawn or restricted. Tobacco must be used 
sparingly, if at all. (2) Climate. In winter the milder temperatures 
of the Southern States, the Riviera, or Egypt, are sought. In summer 
some of the cooler resorts on the seashore or in the mountains of the 
North are recommended. Exposure to cold or wet is likely to induce 
attacks of bronchitis or pneumonia with serious results. (3) Exercise 
must be regulated and hard work of body or mind given up or re- 
stricted. (4) The bowels must be kept open, by laxatives if necessary, 
and the activity of th-e skin promoted by warm baths. Cold bathing 
is forbidden. (5) The regulation of the blood pressure must be care- 
fully considered. If very high, over 200 mm., and especially if accom- 
panied by evidences of cardiac failure, it should be reduced. In milder 
degrees nothing more than the measures already advised is required, 
and even when apparently excessive it may be wisest let alone, since 
it is apparently a protective measure. Severe symptoms, such as head- 
ache, convulsions, or dilatation of the heart, may demand its reduction. 
For this purpose rest in bed and a fluid diet are often effective. In 
emergencies bleeding may be resorted to. Vasodilators are employed, 
most often nitroglycerine in doses of 1/100 grain every two hours, in- 
creased till an effect is produced. The nitrites of sodium or potassium 
are sometimes used instead. Chloral is often valuable, allaying nervous 
symptoms and relieving excessive tension as well. (6) Uremic symp- 
toms call for active treatment. The milder are met by free purgation, 
sweating by hot packs or baths, colonic irrigations, and the use of nitro- 
glycerine. Convulsions demand bromide and chloral, by mouth or rec- 
tum, morphine hypodermatically or chloroform. Venesection is em- 
ployed, especially if the tension is high, and sometimes followed by an 
infusion of salt solution, which while diluting the blood does not mate- 
rially raise the blood pressure. Lumbar puncture has also been em- 
ployed in these cases with good effect, if the quantity of cerebrospinal 
fluid is increased and under high pressure. 

AMYLOID DISEASE OF THE KIDNEY 

Etiology. — Amyloid degeneration of the kidney is always part of a 
general process involving the liver, spleen, and other organs as well. 
The causes are (1) prolonged suppuration, such as occurs in chronic 
empyema, osteomyelitis and the like; (2) late tuberculosis, especially 
the forms involving the lungs and bones, doubtless here also sup- 
puration is the more direct cause; (3) tertiary syphilis. 

Morbid Anatomy. — The kidney is large, the capsule free, the surface 
smooth and pale, the section showing a peculiar smooth, glistening sur- 
face, which on being tested with iodine becomes mottled with patches 
of mahogany-broMOi, representing the scattered areas of amyloid sub- 



FUNCTIONAL EFFICIENCY OF THE KIDNEYS 



169 



stance. In rare instances the kidneys are small, hard, and granular, 
as in interstitial nephritis. 

Symptoms. — Ihe patients are pale and usually edematous. The 
urine varies greatly in specific gravity and amount. It contains large 
quantities of albumin and casts of all kinds. "Waxy casts may be found. 
The liver and spleen are enlarged, palpable, with smooth, firm surface, 
and sharp, hard edge. 

The DIAGNOSIS must rest upon the etiology,, and the combination of 
the urinary conditions with evidence of similar changes in the liver 
and spleen. 

The PROGNOSIS is usually very bad. When the diagnosis is fully 
established, the prospect of life is limited to a few months. 

Treatment. — The underlying condition must be treated. The 
amyloid degeneration is managed on the principles of chronic paren- 
chymatous nephritis. 

CYSTIC DISEASE OF THE KIDNEY 

(1) Cysts develop in the kidney as the result of obstruction in 
many cases of chronic nephritis. They are small and have no clinical 



Fig. 28. Fig. 29. 




Fig. 28. — The cystic kidney, showing multiple cysts with partial preservation of the renal tissue. 
Fig. 29. — The cystic Icidney, showing the kidney converted into multiple cysts with thin walls. 



importance. (2) Solitary cysts of some size may occur and may reach 
such size as to require operation. They are exceedingly rare. Hydro- 
nephrosis from obstruction of the ureter might be classed under this 
heading. (3) True cystic disease of the kidney is congenital, and 
affects both kidneys. The kidneys, by reason of some unexplained 
developmental defect, are converted into a series of cysts of varying 
size, with little or no renal tissue left between thfMn (see Figs. 28 
and 29). The cysts contain dark fluid, which shows albumin, blood 
crystals, cholesterin, and fat droplets, rarely urea. The kidneys may be 



170 



DISEASES OF THE KIDNEYS 



so large and so placed in the pelvis as to obstruct labor ; in the adult they 
may weigh 5 to 6 pounds. 

The SYMPTOMS are those of chronic interstitial nephritis, with 
bilateral tumors in the loins, sometimes large enough to almost fill the 
abdomen. The condition is regarded as congenital, but is often not 
recognized till adult life. 

The only treatment is that of nephritis. 

PYELITIS 

(Pyelonephritis. Pyonephrosis. Surgical Kidney) 

Definition. — An inflammation of the pelvis of the kidney, either 
catarrhal or suppurative. In the latter the process regularly extends 
into the substance of the kidney and constitutes a pyelonephritis, or 
pyonephrosis. 

Etiology. — The disease is of bacterial origin. The bacteria reach 
the kidney through open w^ounds, or from the bladder through the 
ureter (ascending infection), from the blood, or directly from the 
overlying colon. Any influence which lowers the vitality of the patient, 
such as the acute infectious diseases, or any condition causing stagna- 
tion of urine, such as phimosis, enlarged prostate, tumors of the bladder, 
calculi in the pelvis of the kidney or ureter, displacement of the kidney, 
twisting of the ureter, pregnancy, and the like, favors the production 
of pyelitis. 

Morbid Anatomy. — In the milder cases there are swelling and red- 
ness of the mucous membrane of the pelvis and a catarrhal exudate. 
In the severer forms the pelvis is greatly thickened, indurated and 
filled with pus> The straight tubules of the kidney are involved and 
show as radiating whitish or yellow streaks in the cortex. Small or 
large abscesses may be found in the substance of the kidney or the 
whole organ may be converted into one great sac of pus. 

Bacteriology. — In the great majority of cases the colon bacillus is 
found. In others the pyogenic cocci, or any one of a "great variety of 
bacteria, proteus vulgaris and others. 

Symptoms. — In the milder grades there are some slight tenderness 
over the kidneys and the appearance of some few leukocytes with 
mucus in the urine. In the severer suppurative forms the patient 
presents (1) constitutional sjTaptoms of infection, fever, possibly chills 
and sweating, more or less rapid pulse, anemia and emaciation: (2) 
local signs, such as pain and tenderness over the kidney with enlarge- 
ment of the organ and in severe cases rigidity of the overlying abdom- 
inal muscles. 

The COURSE may be either very acute with severe chills and the 
clinical picture of sepsis, or very slow with little or no fever, a little 
pain and tenderness, and gradual loss of vigor. The milder cases 
recover in a few days or weeks. The severer go on to abscess formation 
in the kidney and require Hrainage or removal of the organ. 



FUNCTIONAL EFFICIENCY OF THE KIDNEYS 171 



The BLOOD shows a leukocytosis of moderate or severe grade accord- 
ing' to the reaction to the infection. The ratio of polynuclears will 
be increased, as a rule, in suppurative cases. 

Urine. — The urine is decreased, normal, or increased in amount, 
and the specific gravity varies accordingly. The reaction is acid, neutral 
or alkaline. Pus is present, in large or small amounts ; occasionally it 
may be absent, if the ureter is blocked. Very rarely fragments of kid- 
ney tissue are found. 

Diagnosis. — This must be based on the combined constitutional and 
local signs and the urinalysis. The source of the pus may be inferred 
from the localization of the pain and the tenderness and possibly tumor 
of one kidney. Cystoscopy, or, better still, catheterization of the ureters, 
may show conclusively the side from which the pus comes. The tuber- 
cular forms can be differentiated only by the demonstration of the 
tubercle bacillus in the urine. For conclusive results the organism 
must be tested by inoculation in animals. 

Treatment. — Rest in bed, abundance of water, a nutritious diet, 
and urotropin are employed in the milder cases. Urotropin is given 
in doses of 7 to 8 grains three times daily. If these measures do not 
control the process, the kidney must be incised and drained or removed 
in toto. Vaccines have been tried, but have little effect. 

NEPHROLITHIASIS 
(Renal Calculus. Stone in the Kidney. Gravel) 

Definition. — The deposition of concretions either in the parenchyma 
or pelvis of the kidney. The majority are composed of uric acid and 
its allies, of calcium oxalate, or the phosphates of calcium and mag- 
nesium. A stone is rarely made up of one ingredient, regularly several 
substances are found, with one predominating. 

Calculi. — Stones composed chiefly of uric acid are hard, angular 
and reddish in color. Calcium oxalate also produces very hard calculi, 
usually small in size, gray or blackish in color. The phosphatic stones 
are likely to be soft and whitish in color. Chemical analysis is necessary 
to establish the composition accurately. 

Etiology. — Calculi are met with at all ages, even at birth. Clinically 
they are most frequently seen between 30 and 40 years. The tendency 
to the formation of calculi is transmitted in certain families. The 
causes of the deposition of urinary constituents must vary in different 
cases, as the uric acid and urates are precipitated in acid urine, the 
phosphates in alkaline, and the oxalate of lime in urine, either alkaline, 
neutral, or acid. Errors of diet, the drinking of too little water, and 
lack of exercise are usually given as indirect causes. Excessive eating 
of meat is held to favor the formation of uric acid stones, but there 
is no agreement as to the dietary irregularities underlying the condition. 

Morbid Anatomy. — Stones are single or multiple. They are usually 
found in the pelvis of the kidney, but may be imbedded in its substance. 
Not rarely they are found in the ureter, in Avhich there are three points 



172 



DISEASES OF THE KIDNEYS 



likely to be the location of a stone: (1) jnst at the beginning of the 
ureter, (2) at the crossing of the iliac vessels, (3) the terminal portion. 
The pelvis of the kidney is often dilated, and may show the lesions of 
pyelitis. In advanced cases the kidney is involved and shows the con- 
dition of pyelonephritis. In the absence of suppurative lesions the 
kidney frequently presents an advanced interstitial nephritis. 

Symptoms. — (1) There may be none, although several stones are 
present in the kidney. Pyelitis, hydronephrosis, or chronic nephritis 
may result without symptoms suggestive of stone. (2) Pain more 
or less constant and of varying severity may be present in the affected 
side. The pain is referred to the region of the diseased kidney, or if 
severe may radiate to the other. Nausea, vomiting, or headache, may 
be associated. (3) Attacks of renal cohc may occur. The onset is 
sudden, with violent pain in the affected side, radiating do^^Tiward into 
the scrotum and inner side of the thigh, rarely into the back. Fever 
of 102° to 103° F. follows, and nausea or vomiting results if the pain 
is severe. The urine is passed frequently, but vdth difficulty. The 
patient is usually prostrated during the pain, which lasts for from 
several hours to several days. After one attack the stone may be 
passed and no more follow. Or the stone may remain in the bladder 
and give rise to characteristic symptoms. If the stone remains in the 
pelvis the attacks may be repeated at any time, sometimes frequently, 
in other cases only after years. Pyehtis, hydronephrosis, or chronic 
interstitial nephritis may result. Following the attack of renal colic, 
blood in a trace or considerable amount is usually found in the urine. 
The affected side of the abdomen may be sensitive to pressure and the 
kidney, may feel large. 

Diagnosis. — The location and radiation of the pain are sug^gestive 
only. The presence of blood in the urine with the pain is important. 
Tenderness over one kidney, if present, is usually reliable. Cystoscopy 
is helpful in determining the question of the conditions in the bladder. 
The X-ray is invaluable, regularly locating the stone. Ureteral catheter- 
ization is necessary to determine the functional power of the other 
kidney, if removal of the diseased one is contemplated. The condition 
must be carefully differentiated from appendicitis, gall-stone colic, 
salpingitis, intestinal colic, mucous colitis, or other affections of the 
kidney due to displacement, torsion of the pedicle, or tumor. 

Prognosis. — The attacks of pain or colic are not often grave in 
themselves. Kecurrent attacks may be severe. The development of 
pyelitis, hydronephrosis, or chronic nephritis is of serious import. 

Treatment. — Renal colic, if severe, is best treated by a hot bath and 
an injection of morphine sulphate, 1/6 to Vt gi*ain, or the inhalation 
of a little chlorofonu. Hot poultices or fomentations to the side may 
be used. To prevent the formation of more calculi, a moderate diet 
with abundance of water and reasonable exercise must be prescribed. 
If the composition of the stone is Imowni or can be inferred from the 
exfunination of the urine, the diet can be modified to reduce excess in 



FUNCTIONAL EFFICIENCY OF THE KIDNEYS 173 



urates, phosphates, or oxalates. For uric acid calculi the urine may 
be kept alkaline, for phosphatic calculi acid; and the possibility that 
small stones may be dissolved must be admitted. For large or impacted 
calculi operation is required. Calculi lodged in the lower end of the 
ureter may be dislodged by massage through the rectum. 

HYDRONEPHROSIS 

Definition. — A distention of the pelvis of the kidney, often associated 
with atrophy of the substance of the organ, due to obstruction of the 
ureter and retention of urine. 

Etiology. — The causes are sometimes congenital, such as phimosis or 
stricture of the ureter. It is usually an accident of adult life, due 
to obstruction of the ureter by calculi or twists or tumors, or tumors 
of the bladder, enlarged prostate or stricture of the urethra. 

Morbid Anatomy. — The condition is unilateral unless the obstruc- 
tion is in the urethra. The pelvis is dilated to a greater or less degree 
and the kidney shows corresponding atrophy. In rare cases it is con- 
verted into a mere shell. 

Symptoms. — There may be localized pain and tenderness, especially 
if the obstruction is suddenly developed. In most cases the chief 
symptom is the tumor. This is tense, elastic, and possibly fluctuating, 
if large enough to be definitely palpated. It is often variable, emptying 
and filling again from time to time. It may have the situation of the 
kidney or occupy any part of the abdomen. If large, it may cause 
symptoms by pressure. 

Diagnosis. — The tumor must be differentiated from other cystic 
tumors of the abdomen, ovarian, pancreatic, or mesenteric cysts, and 
distended gall-bladder. 

Prognosis. — Hydronephrosis may exist for years without serious 
symptoms. The greatest dangers are rupture into the peritoneum, or 
suppuration. 

Treatment.— The removal of the cause of obstruction by surgical 
measures is called for. 

PERTNEPHRITIC ABSCESS 

Definition. — A suppurative inflammation of the connective tissue 
about the kidney. 

Etiology. — The disease is usually secondary to suppuration, either 
in the pelvis or cortex of the kidney. It may result from the burro^^^ng 
of an empyema, or an appendix abscess. It sometimes follows trauma, 
such as a blow. 

Morbid Anatomy. — An abscess cavity is formed which may burrow 
upward and involve the pleura, or downward along the psoas and 
present in the groin. The kidney may or may not be involved. 

Symptoms. — The symptoms of the condition are usually v(^ry vague 
until the abscess develops and can be located in the loin. (1) General 
symptoms: fever is present, continued, with moderate remissions, or of 



174 



DISEASES OF THE KIDNEYS 



distinctly septic type (see Fig. 30). The pulse is a little qaickened. 
The patient feels weak and sick. Sweating and anemia may be marked. 

(2) Local symptoms: There is pain in the loin or on one side of the 
abdomen and some rigidity of the abdominal muscles on examination. 

(3) Sooner or later a swelling appears in the loin, with pain and ten- 
derness. Aspiration or incision reveals the presence of pus. The urine 
is usually normal, but if a pyelitis is present will show pus. 

Diagnosis. — This must be based on the general s:yTnptoms of sepsis 
and the local signs of abscess. 




Fig. 30. — Perinephritic abscess with temperature resembling typhoid fever 

Prognosis. — This depends upon the cause. The majority recover 
promptly on the opening of the abscess, but the disease may be fatal. 
Treatment. — Incision with careful drainage is necessary. 

TUMORS OF THE KIDNEY 

Benign tumors of the kidney, such as adenomata, lipomata, fibromata, 
are found at operation or post-mortem, but are not of clinical im- 
portance. Malig-nant tumors, sarcoma and carcinoma, are not infrequent. 
Sarcoma of the kidney is seen from time to time in children, but adults 
are most often affected. Cancer is found only in adult years. 

Symptoms. — (1) The kidney involved increases steadily in size and 
may become rough or nodular. The tumor may press upon or involve 
surrounding organs. (2) Pain is usually present. (3) Hematuria is 
a frequent symptom. (4) Cachexia and emaciation develop. 

Diagnosis. — Tumors of the kidney require to be differentiated from 
those of the liver, spleen, and other adjacent ^dscera. Tumors of the 
adrenal (hypernephroma) are regularly mistaken for renal gro^^i:hs 
and can rarely be satisfactorily distinguished except by the study of 
sections. 

Treatment. — Removal is sometimes successful and should be under- 
taken early. 



IV 



DISEASES OF THE CIRCULATORY SYSTEM 

DISEASES OF THE PERICARDIUM 
PERICARDITIS 

Definition. — An acute or chronic inflammation of the pericardium. 
Several clinical forms are described: (1) Acute plastic, fibrinous or 
dry pericarditis; (2) pericarditis with effusion, serous, purulent, or 
hemorrhagic, and (3) chronic adhesive pericarditis. In both etiology 
and pathology there is a close similarity between pleurisy and peri- 
carditis. 

1. Acute Fibrinous Pericarditis. 2. Pericarditis with Effusion. The 
ETIOLOGY of these two forms is practically the same and as pericarditis 
with effusion is only a further development of the dry or fibrinous 
form they may weU be considered together. The affection develops in 
rare cases primarilj^, but in most instances is secondary. It is met with 
at all ages. (a) Primary or idiopathic pericarditis is a very rare 
affection. Doubtless most of the apparently primary cases are in reality 
secondary to some antecedent infection, especially tuberculosis. (b) 
Secondary pericarditis. (1) Acute rheumatic fever is by all means 
the most common cause. In children pericarditis may develop in in- 
dividuals who have shown very few evidences of rheumatic infection; 
it may follow chorea or the tonsillitis common in rheumatic subjects. 
(2) Scarlet fever, influenza, or pneumonia may be complicated by 
pericarditis. (3) Septicemia, pyemia, or any other type of septicemic 
infection, such as puerperal sepsis, or malignant endocarditis, may cause 
pericarditis. (4) Chronic interstitial nephritis, gout, or diabetes, may 
be followed by pericarditis. (5) Tuberculosis is a frequent cause, 
especially in the generalized type of the disease or in cases of tubercular 
pleurisy. (6) Any acute inflammatory process in the lungs or pleura 
(pneumonia) may by direct extension involve the pericardium. 

Bacteriology. — Some cases of acute pericarditis are sterile, but in 
all probability most of the cases are due to bacterial infection. The 
ordinary pyogenic bacteria, the streptococcus, staphylococcus, pneumo- 
coccus or gonococcus, and the tubercle bacilli are most often found. 

The streptococcus rheumaticus of Poynton and Payne has also been 
found in pericardial effusions. The apparently primary cases are likely 
to yield the tubercle bacillus. The organism is sought by the same 
methods as are applied to pleural fluids. 

Morbid Anatomy. — In the simplest form there is dr^^ fibrinous 
exudate upon one or both surfaces of the pericardium. The fibrin may 
be limited to isolated patches or cover the whole surface. (See Fig. 31.) 
In other cases there is a thick fibrinous exudate coating the heart and 

176 



176 DISEASES OF THE CIRCULATORY SYSTEM 



parietal pericardium and giving a very rough., shaggy appearance to 
the heart. In either case there is a slight exudate of clear or turbid 
serum in the pericardium. The fluid effusion in some cases becomes so 
abundant as to constitute the chief feature of the condition, which is 
then termed pericarditis Avith effusion. The effusion consists of a clear 
or turbid serum or, especially in septic cases, of pus. In rare instances 
blood is present in sufficient amount to tinge the serous or purulent 




Fig. 31. — A heart covered by the thick exudate of fibrinous pericarditis. The upper third of the speci- 
men is the reflected pericardium held by the pathologist's fingers. 

effusion. In all cases of marked inflammation of the pericardium the 
heart muscle is affected to some extent and on examination the myocar- 
dium shows degenerative or inflammatory changes. 

Symptoms. — Acute fibrinous pericarditis frequently gives no dis- 
tinctive s^^mptoms and is disclosed only by careful examination of the 
heart. It is often overlooked and discovered only at autopsy. If 
symptoms are presented they, as a rule, consist of (1) Precordial dis- 



DISEASES OF THE PERICARDIUM 



177 



comfort or pain, usually slight but in some cases severe. (2) Increased 
frequency of the pulse and force of the heart action. (3) Slight 
dyspnea. (4) Fever may be absent, or if present is slight. The 
temperature curve of the primary affection is unchanged or but slightly 
raised. 

2. Pericarditis with Effusion. Like the dry form of the disease 
pericarditis with effusion may develop with few or no distinctive symp- 
toms. The amount of the effusion rather than its character seems to 
determine the severity of the symptoms. (1) Precordial discomfort or 
pain is usually present and may be intense. (2) Dyspnea becomes 
increasingly severe with the accumulation of fluid. Orthopnea is often 
present. (3) Cyanosis, seen especially in the lips and face and under 
the finger-nails, becomes more and more marked. (4) The pulse be- 
comes rapid, small and irregular, in some cases extremely weak or 
imperceptible during inspiration, the so-called pulsus paradoxus. (5) 
The temperature is very irregular. In primary cases there may be an 
initial chill with subsequent high fever. In the secondary cases the 
temperature curve usually shows no definite change, or there may be a 
slight increase. The course of the fever after the establishment of an 
effusion is very variable. The fever continues, as a rule, as long as there 
is any effusion in the pericardium. 

Physical Signs. — (1) Acute Fibrinous Pericarditis. — ^Inspection 
shows nothing significant. Palpation may in marked cases detect a 
friction rub synchronous with systole of the heart, and analogous 
to the friction rub sometimes felt over a dry pleurisy. Percussion shows 
no marked change in the heart area. Auscultation regularly discloses 
a characteristic dry, to and fro, friction sound or murmur produced 
by the rubbing together of the inflamed pericardial surfaces as the 
heart contracts and relaxes. The sound or murmur therefore has the 
rhythm of the heart action. It usually seems superficial, close to the 
ear, and is much harsher and dryer than an endocardial murmur. It 
may be heard over any part of the heart, but most often is detected at 
the base, and is not transmitted beyond the limits of the heart. Similar 
sounds may be produced by pleurisy in the part of the pleura overlying 
the heart. These so-called pleuro-pericardial murmurs are usually easily 
recognized by the fact that they are greatly modified or obliterated by 
having the patient stop breathing during auscultation. If produced in 
the pleura the murmur or rub, as a rule, ceases for a time, to return 
with renewal of respiration. 

(2) Pericarditis with Effusion. — The early signs are commonly 
those of dry pericarditis. As the fluid accumulates the signs are modified. 
Inspection: In children a bulging of the precordial area is frequent. 
In adults the more rigid chest wall does not yield so easily, but the 
precordial area may become prominent. The respiration is rapid and 
superficial with slight motion of the thorax, especially on the left. The 
apex impulse is not visible in the normal site. An impulse may be 
observed in the third or fourth spaces. The diaphragm and left lobe 
12 



178 DISEASES OF THE CIRCULATORY SYSTEM 



of the liver may be depressed and the epigastrium become prominent. 
Cyanosis may be noted in the lips or face and under the finger-nails. 
The expression of the face is often anxious and distressed. Palpation: 
The cardiac impulse is not felt at all or is found in the third or fourth 
space. The friction rub is lost or can be felt only at the base. Fluctua- 
tion cannot be made out through the chest wall. Percussion: The area 
of cardiac dulness is enlarged both to left and right, and if outlined 
on the chest has a characteristic triangular form with a much broader 
base than normal. (See Fig. 32.) The resonance regularly present 
in the fifth intercostal space to the right of the sternum (the cardio- 




FiG. 32. — The enlarged area of cardiac dulness and the obtuse cardiohepatic angle of pericardial 

effusion. 

hepatic angle) is replaced by dulness. If carefully followed the area 
of cardiac dulness is found to increase steadilj^ with accumulation of 
the fluid from day to day, or in severe cases from hour to hour. (See 
Fig. 33.) In any suspected case the outlines of the cardiac dulness 
should be carefully marked upon the chest wall for comparison. Aus- 
cultation : The characteristic feature is the suppression of the cardiac 
sounds. The more abundant the fluid the fainter these become, till they 
can scarcely be heard. If a friction sound has been heard it is lost, 
or limited to the base, but returns with subsidence of the fluid. Signs 
over the left lung: In the left infrascapular region with any large 
effusion, particularly in children, there may be an area of dulness, 
diminished or bronchovesicular voice, and breathing, and diminished 



DISEASES OF THE PERICARDIUM 



179 



vocal fremitus, suggestive of pleural effusion or pneumonia. These 
signs are produced by compression of the left lower lobe. As an effusion 
may be present in the thorax as well as in the pericardium, the differ- 
ential diagnosis is extremely difficult, and doubt can be removed only 
by the careful use of an exploring needle. 

Course and Prognosis. — Acute fibrinous pericarditis regularly runs 
its course in a few days and subsides without serious after-effects. The 
pericardial layers may be left adherent, but unless this is complicated by 
a chronic mediastinal and pleural inflammation, no serious results need 
be expected. 

Pericarditis with effusion runs a very variable course, sometimes 
brief, resolving in a few days, in other cases protracted for weeks or 




Fig. 33. — Outlines of cardiac dulness at successive stages of pericardial effusion, fusing below into 
liver dulness. The X marks the apex impulse; the circles the preferable points for aspiration. 

months. Rheumatic pericarditis regularly resolves, even when the 
effusion is abundant, in the course of two or three weeks. As a com- 
ph cation of pulmonary or pleural inflammation pericarditis with effusion 
adds greatly to the danger of the patient. So long as the effusion 
remains clear the outlook is hopeful, but if, as often happens, the 
inflammation becomes suppurative, the jjrognosis is very grave. In 
unfavorable cases the temperature rises, the pulse fails, cyanosis and 
dyspnea become extreme, delirium and coma develop and death quickly 
follows. In some cases the fatal issue is protracted for weeks and the 
patient dies of exhaustion. 

The Blood.^ — A leukocytosis is present, as a rule, in all forms except 
the tuberculous. The degree of leukocytosis varies greatly and very 
high counts (30,000 to 40,000) may be had in cases with serous effusions, 



180 DISEASES OF THE CIRCULATORY SYSTEM 



but a steady increase in successive counts is always suggestive of the 
development of pus. The differential counts and the cytology of the 
fluid must be interpreted on the same principles as in the case of 
pleural effusions. Serous effusions may be tested for tuberculosis by 
inoculation. 

Diagnosis. — The pericardial friction is the one sure sign of acute 
fibrinous pericarditis. The distinction of this sound from an endo- 
cardial murmur is not difficult. Pleuropericardial sounds may be dis- 
tinguished by the influence of respiration upon them. 

The diagnosis of pericarditis with effusion also rests in great part 
upon the physical signs. The enlarged area of cardiac clulness, the 
dulness in the cardiohepatic angle, faintness of the heart sounds, with 
symptoms of cardiac and respiratory embarrassment, may be confused 
with cardiac dilatation. In the latter the cardiac impulse, though faint, 
is often seen and felt, the sounds are not so faint, endocardial murmurs 
are usually present and the cardiohepatic angle is preserved. A peri- 
cardial friction sound may be heard at the base of the heart, even with 
fluid in the pericardial sac. In cases under observation the surest 
sign of pericardial effusion is progressive enlargement of the area of 
cardiac dulness. This can be determined only by carefully outlining the 
limits of dulness from day to day. 

(3) Purulent Pericarditis. This may follow a serous effusion or 
the exudate may be purulent from the outset. The purulent effusion 
is most often seen in pneumonia, in septic infections and tuberculosis. 
In onset, symptoms and course, it can be distinguished from the serous 
effusion only by the aspirating needle. Various organisms, pneumococcus, 
streptococcus or staphylococcus, or the tubercle bacillus may be found 
in the pus. The prognosis is always grave. 

(4) Hemorrhagic Pericarditis. Blood may be mingled either Avith 
a serous or purulent effusion. Its presence has no peculiar significance 
and does not affect the course or prognosis of the disease. 

Treatment. — Absolute rest is the first requirement. For the relief 
of pain or distress an occasional dose of codeine or morphine may be 
required. To quiet the heart's action an ice cap may be applied over 
the heart. Blisters are now rarely used. The feeding must be carefully 
regulated and the bowels kept open. For large effusions aspiration may 
be required, though it is surprising how often patients with serous 
effusions of considerable amount, especially in the rheumatic cases, 
recover without intervention. Puncture for diagnosis or aspiration is 
made either in fifth right interspace in the fourth or fifth spaces to 
the left, or in the area of cardiac dulness outside the apex, if this can 
be located. The position of the internal mammary arteiy is to be re- 
membered and the needle inserted either close to the sternum or more 
than an inch from it. Aspiration may be repeated. For purulent 
effusions free incision and drainage are necessary. Strs'chnine, digitalis, 
or other cardiac stimulants may be required to strengthen the heart 
action. 



DISEASES OF THE PERICARDIUM 



181 



CHRONIC ADHESIVE PERICARDITIS 
(Adherent Pericardium) 

Chronic Adhesive Mediastinitis. — Following any acute inflamma- 
tion the layers of the pericardium may be left adherent, the adhesions 
being slight or dense. If this be all, no harm results, and in some cases 
the adhesions seem to disappear in time. A condition in which with the 
adhesion of the layers of the pericardium there is combined a chronic 
adhesive inflammation of all the structures in the mediastinum, binding 
the pleura to the pericardium and the chest wall, and to the diaphragm, 
and thus causing the heart to be constantly puUed upon by the ex- 
pansion of the chest in respiration. The heart is regularly found greatly 
hypertrophied and dilated. 

Symptoms. — Simple adhesion of the leaves of the pericardium gives 
no symptoms or signs and is recognized only at autopsy. Chronic 
mediastinitis with adhesions of the pericardium gives no symptoms in 
the early stages, but ultimately causes hypertrophy and dilatation of the 
heart, and the patients come under observation with evidences of 
enlarged heart and signs of cardiac failure, such as dyspnea, cyanosis 
and edema. 

Children or young adults, especially those with a history of rheu- 
matism, are most often affected, and the condition is rarely observed 
among adults. Certain signs are suggestive of it. (1) Retraction of 
the chest wall over the apex or in the epigastrium with systole. (2) 
Systolic retraction of the tenth and eleventh intercostal spaces below 
the angle of the scapula (Broadbent's sign), due to adhesions between 
the diaphragm and the heart, is a valuable sign. (3) Diastolic collapse 
of the veins of the neck ( Freidreich 's sign) may also be observed. (4) 
"With these signs evidences of cardiac failure, dyspnea, cyanosis, rapid 
and irregular pulse, enlargement of the liver and anasarca are usually 
associated. (5) Fixity of the apex impulse with the patient lying on 
his back or side and failure of the left lung to modify markedly the area 
of cardiac dulness on deep inspiration are also evidences of adhesion. 
(6) Auscultation usually reveals the presence of murmurs due to in- 
sufficiency produced by dilatation, mitral systolic, possibly aortic 
diastolic and pulmonary systolic. A murmur indistinguishable from 
that of mitral stenosis has more than once been heard in these cases. 

Diagnosis. — This can rarely be made with any degree of certainty, 
but the condition may be suspected in cases presenting the characteristic 
signs. Adherent pericardium is often discovered only at autopsy. The 
condition is usually regarded as endocarditis with subsequent hyper- 
trophy and dilatation of the heart. Prognosis depends largely upon 
the age and the condition of the heart. In most cases giving clinical 
evidence of the condition the heart muscle is seriously involved and 
the prognosis is bad. Some patients, on the other hand, do well for years. 
The younger the patient, as a rule, the worse the prognosis. Treatment 
is that of the resulting cardiac hypertrophy and dilatation, rest, the use 



182 DISEASES OP THE CIRCULATORY SYSTEM 



of digitalis, cathartics, etc., as necessary. Resection of the ribs and 
cartilages to which the pericardium has become bound has been 
advocated. 

TUBERCULOUS PERICARDITIS 

Tuberculosis of the pericardium is, strictly speaking, always secondary 
to a primary disease in the mediastinal lymph-nodes, the lungs, 
pleura, or other part. When the primary affection is latent, as it may 
well be, in the lymph-nodes, the pericarditis is often spoken of as 
primary. The pericardial affection may be of the dry form or may 
be accompanied by effusion, serous or more rarely purulent. A bloody , 
serous effusion is particularly suggestive of tuberculosis. The clinical 
course of tuberculous pericarditis is likely to be sub-acute or chronic 
in type. The symptoms and signs of the disease are those already 
described for the dry or serous pericarditis or the chronic adhesive 
form. The tuberculous nature of the affection cannot be determined 
on clinical grounds; the diagnosis must rest either on the presence of 
known tuberculosis in the lungs, pleura, or other part, or on the demon- 
stration of the tuberculous character of the exudate, in case fluid is 
obtained. This may be accomplished in the same manner as in pleural 
effusions. (See page 56.) 

Cancerous pericarditis is a rare disease, always secondarv^ to cancer 
elsewhere, particularly of the lungs or pleura. Here also hemorrhagic 
effusions are common. The nature of the disease can be determined 
only by a knowledge of the primary growth. 

OTHER AFFECTIONS OF THE PERICARDIUM 

Hydropericardium. — A non-inflammatory accumulation of serum in 
the pericardium (a transudate). Etiology. — The condition may be part 
of a general anasarca, occurring under the same conditions as hydro- 
thorax. (See page 54.) The symptoms and signs are those of peri- 
carditis with effusion, but without fever, pain, or pericardial friction. 
Increasing dyspnea is usually the prominent feature. The treatment 
is that of the anasarca, or aspiration. 

Chylopericardium is an exceedingly rare condition, like chylous 
ascites, resulting either from disease of the lymphatic vessels (thoracic 
duct) or from a fatty, degeneration of cells in a pericardial exudate. 
The signs are those of pericardial effusion. Hemopericardium, distention 
of the pericardium with blood, results either from penetrating wounds, 
the rupture of an aneurism of the aorta, or a rupture of the heart wall. 
The sjrmptoms are those of hemorrhage with rapid distention of the 
peiricardium. The condition is usually fatal within a few hours. A 
few cases of successful operation for wounds of the heart wall with 
hemopericardium are on record. 

Pneumopericardium and hydropneumopericardium or pyopneumo- 
pericardium are analogous to similar conditions of the j)leura. They 



DISEASES OF THE HEART 



183 



result from penetrating wounds or the rupture of ulcer, cancer or 
tuberculosis, of the stomach, esophagus, or lung into the pericardium. 
Gas may be formed in the pericardium by the action of such organisms 
as the bacillus aerogenes capsulatus. An active pericarditis regularly 
accompanies the condition. The symptoms are those of acute peri- 
carditis with effusion. The signs are those of shifting dulness with 
tympany over the higher portion of the pericardium and remarkable 
churning and splashing sounds with feeble, distant or inaudible heart 
sounds. The prognosis is naturally very grave. The treatment consists 
of incision and drainage of the sac. 

DISEASES OF THE HEART 

ENDOCARDITIS 

Definition. — An inflammation of the endocardium, commonly eon- 
fined to the valves of the heart. 

We describe an acute endocarditis, either simple or malignant, and 
chronic endocarditis. For convenience endocarditis and myocarditis are 
always described separately, but clinically they are very frequently 
associated. 

ACUTE ENDOCARDITIS 

Etiology. — Children are most often affected, but the disease is met 
with at all ages. Two factors are of importance. (1) Infection. Prob- 
ably all cases of acute endocarditis are due to blood infections of some 
kind. Any condition in which, micro-organisms are present in the blood 
may give rise to an acute endocarditis. An acute infectious disease is 
therefore the usual antecedent. Certain acute infections — especially 
those due to cocci — are much more likely to cause endocarditis than 
others. Rheumatic fever causes at least 50 per cent, of all cases, then 
follow pneumonia, septicopyemia, scarlet fever and gonorrheal infection. 
Bacilli, whether typhoid, tubercle, or diphtheritic, though present in the 
blood, rarely cause endocarditis. 

(2) Conditions favoring the lodgment of the organisms on the heart 
valves. Valves damaged by preceding endocarditis are especially vul- 
nerable, so that chronic endocarditis is likely to be complicated by re- 
peated new infections. Valves damaged by trauma or subjected to 
unusual strain are also susceptible. Of the other influences determining 
the lodgment of bacteria on the heart valves, we know little. 

The portal of entry of the bacteria can most often not be determined. 
In rheumatic fever, and possibly other infections, the tonsils are accused. 
Rarely an infected Avound of the surface of the body is followed by 
endocarditis. Uterine infections are most frequently the avenue of 
entrance to the blood and heart. 

Morbid Anatomy. — Vegetations on the heart valves, rarely on the 
heart wall, are the characteristic lesions. The vegetations are commonly 
small, but may be large, wart-like growths. They are composed in the 



184 DISEASES OF THE CIRCULATORY SYSTEM 



early stages of fibrin, leukocytes and often bacteria, later there is a 
growth of connective tissue and a proliferation of the endothelium of 
the heart valve. The mitral and aortic valves are most often affected, 
rarely those of the right side. 

In the severer cases the formation of vegetations is associated with 
ULCERATION (scc Fig. 38), resulting in the destruction of more or less of 
the heart valves. When the heart wall is affected, it may be softened 
or even perforated. With the ulcerative process the vegetations are regu- 
larly larger and more abundant. 

With either large or small vegetations, with or without ulceration, 
vegetations may become loosened from the heart valves and lodge in any 
part of the body, the brain, spleen, kidneys, lungs, etc., and cause the 
usual evidences of embolism. These occurrences are naturally more 
common in severe cases, marked by ulceration and the formation of 
large vegetations. 

As acute endocarditis subsides the vegetations become organized by 
conversion into or replacement by connective tissue, and the valves may 
be deformed by contraction, as in chronic endocarditis. 

Bacteriology.— The cocci are most often found, especially strepto- 
cocci. Staphylococci and pneumococci, rarely gonococci, are occa- 
sionally observed. Bacilli, such as the typhoid, colon, diphtheria and 
tubercle bacilli, are very rarely found. 

While the distinction between simple and malignant endocarditis is 
one wholly of degree, and no sharp line can be drawn between them, 
it serves a useful purpose clinically and is commonly observed. 

SIMPLE ACUTE ENDOCARDITIS 

This includes the type of the disease occurring in rheumatic fever 
and most of the acute infectious diseases. The lesions are mild, the 
symptoms are usually slight, and bacteria cannot, as a rule, be found in 
the blood. 

Symptoms. — These are often entirely lacking or lost in those of the 
primary disease. There may be slight fever, increase of the pulse rate, 
possibly with irregularity, and discomfort or actual pain about the heart. 

Physical Signs. — The significant sign is the development of a mur- 
mur over the mitral or aortic area which is persistent and possibly 
increases with time. The heart may be dilated, its action over-forcible 
or irregular, with a corresponding pulse. Embolic phenomena are very 
rarely met with. 

Course. — The symptoms of simple endocarditis usually subside in 
the course of a few weeks. The affected valve or valves return to nor- 
mal, or they are left permanently damaged and go on to present evi- 
dences of chronic endocarditis. 

Treatment. — Rest is the chief measure. For rapid or excited heart 
action an ice-cap may be applied over the heart. In rheumatic cases 
the salicylates should be given in full doses. The patient must be kept 



DISEASES OF THE HEART 



185 



quiet and nursed with the utmost care till the symptoms and signs dis- 
appear or until the lesion present is thoroughly compensated. This 
may require rest in bed for several months. The diet must be carefully 
regulated to the digestive capacity, and the tendency to anemia met by 
fresh air and iron. Return to active life must be made gradually. 

MALIGNANT ENDOCAKDITIS. SEPTICEMIC ENDOCARDITIS 

Malignant endocarditis differs only in degree from the simple form. 
The difference lies chiefly in (1) that in malignant endocarditis organ- 
isms are regularly found in the blood. From this standpoint the disease 
is therefore a septicopyemia with lodgment of the organisms on the 
heart valves. (2) The formation of vegetations and destruction of the 
heart valves is more pronounced than in the simple form and the dam- 
age done to the heart is therefore regularly greater. The organisms 
found in the blood are strepto-, staphylo- or pneumococci, rarely gono- 
cocci, and still more rarely bacilli, such as the typhoid, diphtheria or 
tubercle bacilli. The streptococcus mitior sen viridans is commonly 
found. 

Etiology. — The disease may complicate any form of septicemia, par- 
ticularly the septic infections of the uterus, infected wounds of any 
kind, pneumonia, or gonorrheal septicemia. In most of the cases no 
source for the septic infection can be found. 

The endocarditis of rheumatic fever rarely assumes the malignant 
type, and the disease is therefore rare in children. Old endocardial 
lesions favor the lodgment of bacteria upon the valves, and doubtless 
for this reason malignant endocarditis is most often seen in early or 
middle adult life in persons having had rheumatic endocarditis. 

Morbid Anatomy. — The vegetations in malignant endocarditis are 
usually large and numerous and the destruction of the heart valves and 
possibly of the heart wall marked. Emboli are numerous in the brain, 
lungs, liver, spleen, kidneys, or possibly in the large vessels of the extrem- 
ities. They appear first as reddish areas of infarction, later becoming 
paler as the blood is absorbed and connective tissue develops or necrosis 
takes place. 

Although pyogenic bacteria are present in these emboli the infarcted 
areas rarely suppurate. Septic meningitis may, however, be caused or 
abscesses in the viscera, the joints, or other parts of the body. The 
characteristic petechial rash may be present on the skin. Anemia is 
often profound. 

Symptoms. — These vary greatly in different cases, the variations 
depending chiefly upon the prominence of the symptoms of septic infec- 
tion and the damage done to the heart. The evidences of sepsis are some- 
times intense and the patients die before much damage has been done 
to the heart. In other cases the septic phenomena are very slight. In 
like manner the evidence of damage to the heart may be either very 
marked or altogether lacking. 



186 



DISEASES OF THE CIRCULATORY SYSTEM 



Several clinical types may be described. 

1. The typhoid type in which the fever, headache, delirium, rapid 
pulse and profound prostration are the marked features. Abdominal 
distention, enlargement of the spleen and diarrhea may also be present 
and the resemblance to typhoid be close. (See Fig. 34.) 

2. The cardiac type in which with the fever and other septic symp- 
toms the heart action is rapid, irregular or intermittent, possibly 
tumultuous; there are loud, harsh murmurs, pain about the heart, and 
possibly dilatation, to direct attention to that organ. 

3. The meningeal type, in which headache, delirium, coma, or con- 
vulsions, rigidity of the neck and general hyperesthesia suggest menin- 
geal involvement. The eruption of malignant endocarditis is often not 
to be distinguished from that of cerebrospinal meningitis. 




Fig. 34. — Malignant (septicemic) endocarditis fever curve resembling typhoid fever. 



4. The chronic septic type, in which the chief feature is a septic 
fever with sweating and progressive anemia lasting for months or even 
a year. Leukocytosis may be lacking in these cases. 

For the diagnosis of malignant endocarditis we require, as a rule, 
(1) Fever, either continuous, or of the remittent or intermittent septic 
type. Leukocytosis may or may not accompany the fever. 

(2) Evidences of endocarditis. These are usually loud, harsh mur- 
murs, most often over the mitral, sometimes over the aortic valves, 
usually murmurs of insufficiency, rarely of stenosis. Dilatation and 
hypertrophy may or may not be present. 

(3) The demonstration of micro-organisms in cultures from the blood. 

(4) The characteristic rash or other embolic phenomena. The rash 
consists of minute red petechial spots, occurring on any part of the 
trunk or extremities, especially on the forearms or the legs. Occasionally 
they are seen in the conjunctivae or on the mucous membranes of the 
mouth and throat. This rash is produced by the lodgment of minute 
emboli in the skin. 



DISEASES OF THE HEART 



187 



Emboli lodging in the brain give rise to partial or complete hemi- 
plegia, paralysis of ocular muscles, etc. In the lung they cause infarc- 
tion with pain, cough, expectoration, possibly bloody, and small areas 
of consolidation. 

In the spleen they cause swelling, pain and possibly a friction rub 
from perisplenitis. 

In the kidneys emboli give rise to complaints of pain and possibly 
hematuria. In the extremities stoppage of the circulation, pallor, cold- 
ness and loss of power are the results. Gangrene may result. 

In characteristic cases the diagnosis may be made on clinical grounds 
alone, but the presence of the micro-organisms in the blood is usually 
necessary to' establish it. The course of the disease varies greatly. Most 
cases are quickly fatal. In the more chronic type life may be prolonged 
for a year or more. Death is nearly always the outcome. A few cases 
of recovery under treatment have been recorded. 

Diagnosis. — From typhoid fever acute cases may be distinguished 
by leukocytosis (20,000 or more), the petechial rash, embolic symptoms, 
and the heart murmurs, while the AYidal reaction is negative and blood 
cultures yield cocci rather than the typhoid bacillus. 

From meningitis the results of lumbar puncture and the blood 
culture usually make the distinction easy. From septicopyemia the evi- 
dence of heart lesions, the characteristic rash or other embolic symp- 
toms "distinguish it. In the chronic type the disease may be confused 
with tuberculosis. Pulmonary signs are usually lacking, there is no 
sputum, or, if present, it does not contain tubercle bacilli, the cardiac 
signs are present and the rash or other embolic symptoms appear sooner 
or later. Malaria may be excluded by the absence of plasmodia and 
the failure of quinine. 

Treatment. — Rest, food, fresh air, are employed as for sepsis of 
any type. In the acute cases morphine may be used for the patient's 
comfort," there being practically no hope of recovery. In the more 
clu'onic type success has been attained in a lew cases by the use of 
autogenous vaccines — that is, vaccines made from the organism obtained 
from the patient's blood after Wright's method. Streptococcus sera 
have also been used in appropriate cases, but with no decisive results. 
Otherwise treatment is purely symptomatic. Transfusion has been re- 
sorted to in cases of profound anemia, and has given rise to temporary 
improvement. 

CHRONIC ENDOCARDITIS 

Etiology. — There are three chief groups of cases : 

(1) Those following acute infectious diseases, especially rheumatic 
fever. At least 50 per cent, of all cases give a history of rheumatic 
infection or chorea. In some instances the development of acute endo- 
carditis during the primary disease is known. In most cases the history 
of rheumatism, scarlet fever, pneumonia, typhoid or other infection is 
the only clue to the cause of the endocarditis. Owing to the frequency 
of acute infectious disease in childhood, the chronic endocarditis of 
those under thirty years of age is usually of this origin. 



188 DISEASES OF THE CIRCULATORY SYSTEM 



(2) Those associated with arteriosclerosis and chronic nephritis and 
due to like causes, especially alcohol, lead, syphilis, or gout. Here also 
age and hard labor are important factors. The endocarditis of this 
type belongs to adult life, and especially to the later decades. 

(3) In many cases it is impossible to ascertain definitely the cause 
of chronic endocarditis. 

Morbid Anatomy.— The valves of the left heart are regularly 
affected, those of the right side rarely. The affected valves are thickened, 
opaque, shrunken, sometimes the various cusps or leaflets are adherent 
and variously distorted. In the auriculo-ventricular valves the changes 
in the valve leaflets are accompanied by thickening and retraction of 
the chordse tendinese, which greatly augment the effect of the changes 
in the segments of the valves. In the late stages of the chronic endo- 
carditis the valves may become extensively calcified. 

Vegetations such as appear in acute endocarditis may be found at 
any stage of the more chronic process and ulceration at times occurs, 
especially in advanced cases. 

As a consequence of chronic endocarditis the chambers of the heart 
are regularly dilated to a greater or less extent and the walls thinned 
or thickened. Atheromatous changes in the cardiac arteries are com- 
monly present, especially in the chronic endocarditis associated with 
arteriosclerosis, together with more or less pronounced changes in the 
myocardium (chronic myocarditis). Chronic nephritis, usually of the 
interstitial type, is also commonly associated. 

EFFECTS OF CHRONIC ENDOCARDITIS. CHRONIC VALVULAR 
HEART DISEASE 

The Valves of the Heart. — These are rendered incompetent or in- 
sufficient so that they no longer properly close the orifices they guard 
or they are narrowed or stenosed so that they obstruct the flow of the 
blood through them. Frequently both results are produced. The fur- 
ther effects of insufficiency or stenosis of any valve of the heart vary 
with the valve affected, the degree of the defect, insufficiency or stenosis, 
and the secondary changes produced in the chambers of the heart. The 
heart is a living pump whose satisfactory operation depends not only 
on the integrity of its valves and chambers, but upon the maintenance 
of a normal circulation of blood in its walls and also upon normal 
innervation. The effects of valvular lesions are therefore not adequately 
stated in purely mechanical terms and yet a clearer understanding of 
them may be had by tracing out the physiological results of valvular 
defects. This may best be done with the aid of the accompanying dia- 
grammatic representation of the relations of the cardiac chambers and 
valves. (See Fig. 35.) 

Aortic InsufBciency. — When the aortic cusps are rendered insuffi- 
cient, a part of the blood thrown into the aorta by the systole of the 
ventricle is allowed, during the diastole, to flow back into the left 



DISEASES OF THE HEART 



189 



ventricle, while at the same time this ventricle is receiving its usual 
charge from the auricle. The result is in the first place to overfill the 
ventricle and so dilate it and secondly by increasing the amount of blood 
to be thrown out, that is, increasing the w^ork, to cause hypertrophy. 
These two changes go hand in hand and in the case of aortic insufficienc}^ 
the dilatation and hypertrophy of the left ventricle are marked and 
often extreme, producing the so-called cor bovinum. 

Dilatation of the left ventricle, when marked, enlarges the left 
auriculo-ventricular ring to such an extent that the mitral valve can no 
longer properly close it and a relative mitral insufficiency results, though 
the valve may be perfect. Aortic insufficiency is therefore regularly, 




Fig. 35. — A diagrammatic representation of the heart. V C, the vena cava; yl, right auricle; F, 
right ventricle; P, pulmonary valves; L A, left auricle; L V , left ventricle; A, aortic valve. 

in its advanced stages, complicated by mitral regurgitation, and from 
one point of view a mitral insufficiency may prove advantageous to the 
patient with aortic insufficiency by lessening the work to be done in 
emptying the ventricle at each systole. Once mitral insufficiency is 
produced the heart is subject to the changes incidental to this lesion, 
just as much as though the insufficiency had been produced by disease 
of the valve itself. 

Mitral Insufficiency. — Incompetence of the mitral valve allows the 
left ventricle in systole to empty itself not only into the aorta but 
into the auricle as well, and thus temporarily at least lessens the work 
of the ventricle. But the left auricle thus unnaturally fill(Ml both from 
the left ventricle and from the right through the i)uliii()iuiry vessels, 
systole of the two ventricles being synchronous, must first dilate and 



190 DISEASES OF THE CIRCULATORY SYSTEM 



hypertrophy. By such changes the circulation is for a greater or less 
time maintained practically normal. 

Sooner or later, however, the efficiency of the auricle fails, the blood 
collects in the lungs, the pressure in the pulmonary artery rises, dila- 
tation and hypertrophy of the right ventricle follow ^vith possible incom- 
petence of the tricuspid valve, and ultimately dilatation and hypertrophy 
of the right auricle. 

Aortic Stenosis. — The difficulty in stenosis of the aortic valve lies 
in the- increased force required to empty the ventricle through the nar- 
rowed orifice, and consequent imperfect emptying of the ventricle. 
Hypertrophy and dilatation of the ventricle follow as in aortic insuffi- 
ciency, but they are less marked and never reach the extreme limits seen 
in the latter condition. Dilatation of the auriculo-ventricular ring may 
produce mitral insufficiency and all the chain of events already described. 

Because of their close relation to the cusps of the aortic valves the 
coronary arteries are very likely to be involved in cases of aortic dis- 
ease, and narrowing or obliteration of the smaller branches results in 
fibrous changes in the myocardium. 

Mitral Stenosis. — This lesion directly increases the work demanded 
of the left auricle, with resulting dilatation and hypertrophy and an 
early development of pulmonary congestion, hypertrophy and dilatation 
of the right ventricle, and incompetency of the tricuspid which must 
naturally follow. The left ventricle, on the other hand, remains of nor- 
mal size. The hypertrophy of the heart in mitral stenosis is demon- 
strable, as a rule, only on the right side. The auricular enlargement, 
because of the relation of the left auricle to the chest wall, is rarely 
shown by physical examination. 

Primary right-sided lesions such as pulmonary stenosis or tricuspid 
insufficiency cause dilatation and hypertrophy of the right chambers in 
a manner analogous to that in which these changes develop secondarily 
to the lesions of the left side. 

Compensation. — When in any cardiac lesion the resulting changes 
in the heart, hypertrophy and dilatation, permit the circulation to be 
carried on approximately normally, the lesion is said to be compensated 
and the process is spoken of as compensation. Eventually in most cases 
of chronic endocarditis, either by reason of increasing dilatation, or 
because of changes in the heart muscle or the coronary arteries, the 
heart becomes incapable of maintaining a normal circulation, and symp- 
toms of cardiac distress and failure of the circulation follow. We then 
say that compensation is broken. 

Compensation and Failure of Compensation. — In the stage of 
compensation we may say there are no symptoms, but this statement 
must always be made with certain reservations. The heart with 
damaged valves whose defect is relatively balanced by dilatation and 
hypertrophy of the chambers will often do its work perfectly, so long 
as the patient leads an inactive life, but in most cases any unusual exer- 
tion, especially running or climbing stairs, will cause dyspnea, palpi- 



DISEASES OF THE HEART 



191 



tation and possibly cyanosis, more readily than in the normal individual. 
So long as these symptoms of distress occur only under unusual con- 
ditions they are ordinarily disregarded. When they appear under the 
ordinary conditions of life, they are regarded as signs of failing 
compensation. 

It is possible that a heart with damaged valves be so adjusted by nat- 
ural changes that it will do its work even under the severest trial as 
well as a normal heart. In an instance within the writer's knowledge 
a student with marked signs of mitral insufficiency, after being warned 
that he should not enter the contest on account of his cardiac condition, 
won a mile race against a number of rivals and with less distress than 
any of them. Such instances of perfect compensation are, however, very 
exceptional. 

Failure, or breaking of compensation, may be caused in several ways : 
(1) By advancing changes in the heart valves, increasing steadily the 
inefficient action of the heart; (2) by any influence which increases 
blood pressure, especially sudden or severe physical exertion, progressive 
arteriosclerosis, chronic Bright 's disease, and the like ; ( 3 ) by weakening 
of the cardiac muscle, (a) chronic progressive changes in the cardiac 
muscle are found in most cases of chronic endocarditis. Such myo- 
carditis gradually impairs the efficiency of the heart muscle, and often 
in the end determines the failure of compensation. IMyocarditis is most 
marked in those cases of endocarditis in which arteriosclerosis of the 
coronary arteries is regularly found, i.e., in endocarditis involving the 
aortic valves, (b) Apart from definite myocardial changes the vigor of 
the heart muscle may be impaired as that of any part of the body by 
many influences, especially impaired nutrition from any cause, anemia, 
acute disease, such as pneumonia or typhoid fever, and the like. Failure 
of compensation is therefore often a direct result of intercurrent acute 
disease. 

In any of these ways the compensated heart may be rendered unable 
to longer perform its functions satisfactorily and sj^mptoms develop. 
The symptoms of broken compensation depend upon the over-strain of 
the heart and the circulatory changes induced by venous congestion. 
By reason of the failing power of the left heart the blood pressure falls 
in the arteries, the difference of pressure between arteries and veins 
is less than normal, and the blood therefore tends to accumulate in the 
veins. If the right heart is also affected, the aspirating action of the 
right chambers on the great veins is lessened and the tendency to 
venous stagnation is further augmented. 

The venous congestion of cardiac failure usually shows itself first 
in the most dependent portions of the body, the feet and legs, later in 
the abdomen and the abdominal viscera, especially in the parts drained 
by the portal vein, then in the lungs and pleura, and finally in the 
hands, arms and even in the face and neck. 

As the venous congestion increases in any part there is a tendency 
to the exudation of serum from the blood-vessels, with resulting edema. 



1J2 DISEASES OF THE CIECULATORY SYSTEM 



In the peritoneal, pleural or pericardial sacs sncli edema is regularly 
accompanied by an accumulation of free fluid constituting ascites, 
hydrotliorax, or liydropericardium. 

Chronic congestion of the mucous membranes causes a chronic catar- 
rhal intlaimnation which is attended with characteristic changes in 
structure and function. In the lungs a chronic bronchitis is produced. 
In the alimentary tract chronic gastritis and chronic enterocolitis. 

Chronic congestion of the liver, spleen and kidneys results in en- 
largement with chronic interstitial inflammation and consequent fibrosis. 

In the lungs a similar condition of chronic interstitial inflammation, 
commonly called bro^m induration, often results. 

Symptoms of Chronic Endocarditis. — ^Vlien compensation fails in 
chronic endocarditis, symptoms develop either suddenly or gradually, 
depending upon the causes initiating the failure. Whatever the lesion 
the sjTQptoms of failure are in general produced by progressive venous 
stasis in the lungs, liver, abdomen and extremities, and the clinical 
picture is modified but little by the particular valvular lesion. It seems 
best, therefore, to first describe the common picture of cardiac failure 
and later indicate the modifications produced by particular lesions. 

(1) The heart itself reacts to its increasing burden by producing 
more or less discomfort or actual pain, by more rapid action, either 
feebler or more forcible, and by palpitation. In the later stages the 
action of the heart becomes irregular and intermittent. 

(2) Pulmonary congestion declares itself by increasing dyspnea, 
cough, expectoration and cyanosis. At first the dyspnea is excited only 
by exertion, especially running or climbing, later it is present even at 
rest. Often the patient is forced to sit up on account of the dyspnea 
(orthopnea). Xot infrequently the dyspnea is paroxysmal, "cardiac 
asthma." 

The early cough is slight, and attended only by mucous expectora- 
tion. Constant coughing and blood-tinged or bloody expectoration mark 
the severer conditions. These symptoms are often aggravated by the 
development of hydrothorax. In the final stages pulmonary edema may 
occur, with profuse watery exudation into the trachea and bronchi, pro- 
ducing intense dyspnea and cyanosis, with characteristic physical signs. 
Pulmonary edema is the common precursor of death. The sputum in 
pulmonary congestion often shows blood cells or epithelial cells contain- 
ing blood pigment. 

Cyanosis first shows itself only after exertion under the finger- 
nails or in the lips, later it appears in the skin and is seen even at rest. 

(3) The gastric and intestinal congestion produce loss of appetite, 
nausea or vomiting and constipation, rarely diarrhea. These symptoms 
vary with the severity of the condition. If vomiting occurs, the vomitus 
consists of food, or food and mucus. Traces of blood may be seen, but 
hematemesis is rare. The abdomen may be distended and all these 
symptoms augmented by the presence of ascites. 

(4) The urine becomes scanty, high-colored, and of high specific 
gravity, with a trace of albumin and hyaline or granular casts. Blood- 



DISEASES OF THE HEART 



193 



cells may be found at any time or a pronounced hematuria may be 
caused by emboli. 

In the extremities edema shows itself, at first appearing only after 
standing, later becoming constant and extending to the legs, the trunk, 
hands, arms, and even the face. 

I. MITRAL INSUFFICIENCY 

Insufficiency of the mitral valve is the most frequent result of chronic 
endocarditis. It is met with at all ages, but especially in children. It 
develops in the course of chronic endocarditis, either from thickening 
and shrinking of the leaflets of the valve or from retraction caused by 
shortening of the chordae tendinese. 

Symptoms. — Mitral insufficiency is one of the most easily compen- 
sated lesions, often existing for many years without symptoms. Com- 
pensation, once thoroughly established, may be protracted indefinitely. 

Mechanics. — When the mitral valve is insufficient, a part of the 
contents of the left ventricle will, on systole, be forced back through 
the leaking valve into the left auricle. This chamber must therefore 
dilate and, in the effort to drive forward an increased charge, hyper- 
trophy. By reason of these changes, it will gradually become capable 
of driving into the ventricle a larger quantity of blood with each systole. 
The ventricle will, therefore, gradually dilate and hypertrophy. 

The filling of the auricle in diastole not only from the pulmonary 
veins but also in part from the ventricle raises the tension in the 
auricle and gradually in the pulmonary vessels. The right ventricle 
therefore dilates and hypertrophies and the series of changes on the 
right side already described (see p. 181) is initiated. 

Physical Signs. — Inspection. — The precordial region may be promi- 
nent or bulge by reason of the hj^pertrophj^ of the left heart, especially 
in children. The apex impulse is displaced downward and outward to 
a moderate degree. Palpation. — The impulse is forcible, or in extreme 
cases heaving in character. A systolic thrill is said by some to occa- 
sionally accompany mitral insufficiency. There is doubt of this. It is 
difficult to exactly time a thrill at the apex, and also a certain degree 
of roughening or narrowing of the valve (stenosis) often accompanies 
insufficiency. A thrill, presystolic in time, is characteristic of mitral 
f^tenosis. Percussion. — The area of deep cardiac dulness is enlarged to 
the left, usually to a moderate degree. Auscultation. — At the apex a 
loud, blowing, systolic murmur is heard, either replacing or accompany- 
ing the first sound. The murmur is regularly transmitted in all direc- 
tions to some extent, but especially to the left, and may easily be heard 
in the back. 

The second sound over the pulmonic valve is accentuated, owing to 
the increased tension in the pulmonary artery. In the later stages 
there may be evidences of hypertrophy of th(' right ventricle, pulsation 
in the epigastrium and increase of cardiac dulness to the right of the 
sternum, or even of tricuspid regurgitation. 
13 



194 DISEASES OF THE CIRCULATORY SYSTEM 



The pulse is usually regular and of moderate volume but low ten- 
sion. Only in the late stages does it become irregular or intermittent. 

Prognosis. — Mitral insufficiency is probably better borne than any 
other valvular lesion. In well-compensated cases it may have little 
influence upon the duration of life. In children, however, any valvular 
defect is of serious import, because of the difficulty of preventing over- 
exertion in play or sports and consequent disturbances of compensation. 

Diagnosis. — There are two conditions likely to mislead: (1) Acci- 
dental or hemic murmurs systolic in time and softly blowing in char- 
acter, heard at the apex and possibly transmitted to some distance 
from the apex. Such murmurs are met with in the various fevers and 
anemias and disappear with recovery from the fever or anemia. With 
such murmurs there is no hypertrophy of the ventricle, no accentuation 
of the second pulmonic sound, and the murmur itself is softer in quality 
than those produced by organic lesions. (2) ]\Iitral insufficiency pro- 
duced by dilatation of the left ventricle, the so-called relative incompe- 
tence of the mitral valve. All the signs of mitral insufficiency are found 
in this case, and only the knowdedge of the sequence of events leading 
up to the development of the murmur or the presence of a presystolic 
murmur indicative of an accompanying stenosis of the valve will 
enable one to definitely decide the question. Thus if the murmur of 
mitral insufficiency develops secondarily to an aortic lesion, either 
insufficiency or stenosis, or to the increasing strain of high arterial 
tension from any cause, it can safely be set down as due to dilatation. 
If, on the other hand, the murmur of mitral insufficiency is accompanied 
by that of stenosis, it is surely due to disease of the mitral valve itself. 

II. MITRAL STENOSIS 

This lesion, in a pure form^ is a less frequent type of chronic 
endocarditis. A certain degree of stenosis often develops in the course 
of mitral insufficiency and the two conditions are frequently associated. 

]\Iitral stenosis is most often met with in women in early adult life. 
It is not often found in childhood or at advanced age. It is one of the 
most serious of the valvular lesions. 

]\Iechanics. — Narrowing of the mitral valve dams back the blood in 
auricular systole and opposes the normal onward flow. The left auricle 
therefore hypertrophies and emptying itself incompletely dilates; 
pressure rises in the pulmonary circuit, and dilatation and hyper- 
trophy follow on the right side. The left ventricle remains of normal 
size, and often appears contracted in comparison with the enlarged 
other chambers. 

The symptoms are those already described, but in mitral stenosis 
signs of pulmonary congestion, dyspnea, cough, and cyanosis are likely 
to appear early and the pulse is frequently very small and irregular 
or intermittent. 

Physical Signs. — Inspection. — The precordium is usually normal. 
The apex impulse is not displaced, unless by reason of hypertrophy on 



DISEASES OF THE HEART 



^195 



the right side. Cyanosis of the finger-tips or the lips is early noticeable. 
There may be prominence of the lower sternum and an epigastric pulsa- 
tion from hypertrophy of the right ventricle. Palpation confirms the 
findings of inspection. The apex impulse is not forcible. The heart 
action is often feeble, irregular or intermittent. A short, rumbling, 
presystolic thrill is regularly felt at the apex, ending in a sharp shock 
as the ventricular systole begins. Percussion shows little or no increase 
in the cardiac dulness to the left, a definite increase to the right, as a 
rule. The pulse is small, and often irregular and intermittent. 

Auscultation. — A short, rough, rumbling presystolic murmur closely 
limited to the apex is characteristic of mitral stenosis. The murmur 
increases in intensity and ends in a short, sharp first sound or merges 
into the blowing systolic murmur of a complicating insufficiency. 

The murmur is, of course, due to the passage of blood through the 
narrowed orifice under the impulse of auricular systole. When com- 
pensation fails and the auricle dilates, the murmur may disappear, 
to return with recovery of auricular power. In the absence of the char- 
acteristic murmur, the sharp first sound and the accompanying shock, 
together with the other signs, may enable one to make the correct 
diagnosis. 

Diagnosis. — In its typical form mitral stenosis is easily recognized, 
yet it is well known that this lesion is very frequently overlooked. 

The characteristic murmur may be absent as indicated above, but 
the presence of the other signs should lead to a correct diagnosis. 

Two other conditions give rise to murmurs not easily distinguished 
from that of mitral stenosis. (1) The so-called Flint murmur, accom- 
panying aortic insufficiency. This is a diastolic or presystolic rumble 
heard at the apex and attributed to the impact of the regurgitated blood 
upon the large anterior segment of the mitral valve, causing it to flap 
and possibly interfere with the free entrance of blood from the auricle. 
The association of this murmur with that of aortic insufficiency should 
put the observer on his guard. It occurs in many cases of aortic insuffi- 
ciency, while true mitral stenosis is very rarely indeed combined with 
that lesion. The sharp apical first sound and the accentuated second 
pulmonic are not heard in aortic insufficiency. 

(2) In adherent pericardium a murmur indistinguishable from that 
of mitral stenosis has more than once been heard and has led to error 
in diagnosis. The reasons for this have not yet been given. 

Prognosis. — Mitral stenosis is a grave lesion, but may be well borne 
for many years. When signs of failure once develop, restoration is 
difficult, because the strain falls upon the thin-walled auricle and the 
relatively weak right ventricle. Patients with this lesion rarely reach 
old age. 

III. AORTIC INSUFFICIENCY 
Aortic insufficiency ranks next to mitral insufficiency in frequency. 
It is most often found in men, especially in middle life. It may be 
produced in different ways: (1) Most frequently it results from an 



196 



DISEASES OF THE CIRCULATORY SYSTEM 



endocarditis, rheumatic in origin, involving the aortic cusps, thickening 
and contracting them and uniting their edges, or actually destroying 
portions of the valves. 

(2) It may be part of a general arteriosclerosis affecting particularly 
the arch of the aorta and the adjacent valves. In these cases extensive 
calcareous degeneration of the aorta and valves is frequently found. 

(3) Segments of the valve may be ruptured by extreme physical 
exertion, such as lifting heavy weights, v^ith resulting insufficiency. 
This lesion is therefore common in men engaged in laborious occu- 
pations. In animals similar conditions can readily be produced by 
cutting or tearing one cusp of the valve. 

(4) A relative incompetency of the semilunar valves may be pro- 
duced by dilatation of the aorta due to arteriosclerosis and high arterial 
pressure, especially in cases in which there is an aneurism of the ascend- 
ing aorta. 

Mechanics. — In aortic insufficiency part of the blood thrown into 
the aorta by systole of the left ventricle is allowed by the imperfect 
closure of the semilunar valves to flow back into the ventricle in 
diastole. The ventricle therefore fills from both sides, the auricle and 
the aorta. It must therefore promptly dilate and, having to move an 
unusual charge of blood, hypertrophy. Extreme grades of hypertrophy 
and dilatation of the left ventricle are therefore seen more often in 
aortic insufficiency than in any other condition. The large amount of 
blood thrown with each systole of the enlarged ventricle into the aorta, 
and the rapid disappearance of the wave, partly forward into the distal 
arteries and partly backward into the ventricle, give rise to unusual 
oscillations in the contents and pressure in the arteries. 

Symptoms. — By reason of the relations between the aortic valves 
and the cerebral arteries the oscillations in the blood stream affect par- 
ticularly the circulation in the brain. Complaints of headache, dizzi- 
ness, flashes of light, or faintness upon rising suddenly are rather char- 
acteristic of the lesion. The coronary arteries rising from the aorta 
immediately behind the cusps of the aortic valve are likely to be involved 
in any process affecting the valves, and patients with aortic insufficiency 
are therefore more liable to suffer severe cardiac pain or to die of 
angina pectoris than are those with other forms of valvular disease. 

Aortic incompetency may long be well compensated by change in 
the left ventricle. The circulation is therefore well maintained and 
these patients often show no traces of cyanosis till late in their disease 
the ventricle begins to fail and stasis occurs in the pulmonary and 
peripheral circulation. 

Physical Signs. — Inspection. — The preeordium is prominent or 
bulges. The apex impulse is displaced outward and downward, in 
some cases to an extreme degree, aortic insufficiency producing the larg- 
est hearts {coi- hoviiwim) one sees. The impulse is often widely diffused 
and heaving in chnrnctiM'. The unusual pulsation of the arteries, espe- 
cially in the neck, is easily observed. If the patient's hand be raised and 



DISEASES OF THE HEART 



197 



gentle pressure made upon the edge of a finger-nail the red margin will 
be seen to advance rhythmically with the beat of the heart upon the 
whitened area (capillary pulse). Similar phenomena may be observed 
in the uvula or even in the skin of the forehead, if the latter be rubbed 
to cause flushing. Remarkable pulsation in the retinal arteries may 
also be observed by the ophthalmoscope. 

Palpation. — The displaced apex and its forcible impulse may be felt. 
The unusual pulsation of the arteries is also noted and not infrequently 
a thrill is to be felt over the larger arteries, such as the femoral, 
brachial, radial, or those of the neck. A diastolic thrill may be felt in 
the aortic area. 

Percussion. — The area of deep cardiac dulness is enlarged greatly 
to the left and downward, corresponding to the position of the apex. 
The right side of the heart is not affected till late in the disease. The 
transverse area of cardiac dulness is greater in aortic insufficiency than 
in any other lesion. 

Auscultation. — The characteristic murmur of aortic insufficiency is 
diastolic in time, heard best in the second intercostal space just to the 
right of the sternum and transmitted downward under the sternum and 
along its left margin, even to the ensiform cartilage. Often the murmur 
is not loudest at the expected site, but at some other point along the 
course described. It may also be transmitted upward to the clavicle. 
Over the arteries susceptible of auscultation both systolic and diastolic 
murmurs may often be heard. The second aortic sound is regularly 
replaced by the murmur ; the second pulmonic is heard as usual or may 
be accentuated. Since roughening of the aorta often accompanies aortic 
insufficiency, a systolic murmur may be heard at the base and upward 
over the great vessels, apart from stenosis of the valve itself. 

The pulse of aortic insufficiency is one of its most characteristic 
features, the explanation of which has already been given. The artery 
rises and falls under the finger with an unusual amplitude and sudden- 
ness of expansion and recoil, the so-called water-hammer or Corrigan 
pulse. The sphygmomanometer shows that there is a corresponding 
sharp rise and fall in blood pressure, the systolic being unusually high, 
the diastolic unusually low. 

Diagnosis. — Slight degrees of aortic insufficiency may be over- 
looked. The murmur is often soft and faint, not to be heard over the 
usual site, but audible on careful examination along the left margin 
of the sternum or even at the ensiform cartilage. 

The hypertrophy of the heart and the rapid bounding pulse of 
exophthalmic goitre sometimes suggest aortic insufficiency. The capil- 
lary pulse may also be seen in this condition. The characteristic mur- 
mur is, however, absent and the second aortic sound is accentuated. 

Prognosis. — Aortic insufficiency is a severe lesion, but inasmuch 
as the strain falls directly on the strong left ventricle it is often well 
borne for years. On the other hand, where it is produced by a chronic 
and progressive endocarditis the symptoms of circulatory disturbance 



198 



DISEASES OF THE CIRCULATORY SYSTEM 



are often severe and the course short. Aortic insufficiency in advanced 
years is especially likely to be complicated by attacks of angina pectoris 
any of which may be fatal. 

IV. AORTIC STEXOSIS 

Stenosis of the aortic valve is a relatively rare lesion. It most often 
occurs in association with general arteriosclerosis in men past middle life. 

The stenosis is produced by thickening, adhesion and contraction 
of the valve. The normal opening may be reduced to a narrow slit. 
Involvement of the coronary arteries and resulting myocardial changes 
are common. 

Mechanics. — The emptying of the left ventricle in systole is im- 
peded, with resulting hypertrophy and dilatation. In the elfort to com- 
pletely empty itself the ventricle takes more than normal time. Systole 
is therefore prolonged and the pulse is often slow. The pulse is also 
small, the artery contracted and hard. Eventually the left ventricle 
dilates, the mitral valve becomes relatively incompetent and the usual 
course of broken compensation is followed. 

Symptoms. — Cerebral s^onptoms due to inadequate supply of blood 
to the brain are common. The patient suffers from headache, vertigo, 
or insomnia. The pulse is often slow. Otherwise the symptoms are 
those common to valvular lesions. 

Physical Signs. — Inspection. — The apex is displaced clo^^Tiward and 
outward, but to a less degree than in insufficiency of this valve. The 
precordium may be prominent and the impulse slow and heaving, or 
full. Palpation confirms these evidences of hypertrophy of the left 
ventricle. There is usually a marked thrill, systolic in time, felt over 
the aortic area and transmitted upward along the great vessels to the 
clavicle, possibly beyond. 

Percussion. — The area of deep cardiac dulness is increased to the 
left and downward to a moderate degree. Only in late stages will there 
be any increase to the right. In the aged the increase in size of the 
heart is often obscured by pulmonary emphysema. 

Auscultation. — A long, harsh, "sawing" murmur is heard over the 
sternal end of the second right intercostal space and to some extent 
round-about, but particularly upward over the great vessels to the 
clavicle. The aortic second sound is obliterated or replaced by the 
diastolic murmur of incompetency. 

The pulse of aortic stenosis is small, the artery contracted and hard. 
Often the rate is slow and irregular, especially in elderly persons. 

Diagnosis. — The murmur of aortic stenosis may be simulated by 
roughening of the aorta without involvement of the valve. In such 
cases the ventricle should be less hypertrophied. and the second aortic 
sound should be clear, or even accentuated. 

Accidental or hemic murmurs may also be heard over the aortic 
area, but the absence of other signs of organic lesion should prevent 
mistakes. 



DISEASES OF THE HEAET 



199 



V. PULxMONARY INSUFFICIENCY 

This lesion is one of the rarest forms of valvular disease. It may 
result from congenital malformation, from acquired endocarditis and 
possibly as the result of high tension in the pulmonary artery. It is 
therefore a possible result of dilatation and failure of the left heart, 
but as a matter of fact is extremely rare in that relation. 

The SYMPTOMS depend upon failure of the right ventricle and con- 
gestion of the liver, and the extremities of the body should be especially 
marked. 

Physical Signs. — A blowing diastolic murmur in the second left 
intercostal space close to the sternum and transmitted downward along 
its left margin, together with signs of dilatation and hypertrophy of 
the right ventricle, is characteristic. 

VI. PULMONARY STENOSIS 

Narrowing of the pulmonary valve, while a possible result of ac- 
quired endocarditis, is almost unknown in that relation. It is, however, 
the most common form of congenital lesion consistent with life beyond 
infancy. It is therefore the most common congenital lesion met with 
clinically. Persons with this lesion have been known to reach the age 
of 45 years. 

The lesion is produced by a fusion of the semilunar cusps, so that 
all evidences of separation may be obliterated, and the orifice reduced to 
a diameter of two or three millimeters. The right ventricle will be 
hypertrophied and dilated and the tricuspid valve probably incompe- 
tent. The foramen ovale is always patent in congenital cases and the 
interventricular septum often defective. 

Symptoms. — Cyanosis on the slightest exertion, or after eating, or 
even at rest, is the most striking symptom. The cyanosis is often of 
extreme grade, and yet the patients may be comparatively comfortable 
and able to get about easily. Deep cyanosis with such comparative 
comfort is seen otherwise only in advanced emphysema with dilated 
right heart or in those poisoned by large doses of coal-tar preparations. 
With the cyanosis there are dyspnea on exertion, cough, debility, a 
tendency to disturbances of digestion, and finally general anasarca. 

Physical Signs. — Inspection. — The cyanosis is the obtrusive sign. 
It is especially evident in the lips and fingers, which are clubbed"; that 
is, the terminal phalanges are unduly large. When the patient is lying 
down, the cyanosis may be but slight, but becomes marked in the 
upright position or on exertion. It varies greatly from time to time. 
There may be pulsation in the epigastrium or bulging of the precordium 
from hypertrophy of the right ventricle. 

Palpation. — The signs of hypertrophy of the right ventricle may 
be confirmed, the apex may be somewhat displaced to the left, the im- 
pulse is that of the right ventricle. 

A rough thrill, harshest over the pulmonic area, and transmitted 



200 



DISEASES OF THE CIRCULATORY SYSTEM 



widely m all directions, but particularly upward and to the left in 
the line of the palmonary artery, is felt with systole. 

Percussion. — The area of cardiac dulness is increased especially on 
the right. 

Auscultation. — The murmur in pronounced pulmonary stenosis is 
the loudest and harshest ever heard. It may easily be appreciated by 
the ear near to but not touching the chest, and in the ordinary case can 
be heard at any point on the chest, front or back. Like the thrill, it 
is loudest over the pulmonic valve and in the line of the pulmonary 
artery. The second pulmonic sound is absent, because of the fusion of 
the cusps of the valve and the low tension in the artery. 

Diagnosis. — The history of cyanosis from birth, the murmur, thrill 
and enlarged right heart give an almost perfect clinical picture. The 
only condition which gives similar signs is the patent ductus Botalli. 
The accentuation or absence of the second pulmonic sound is the 
strongest point in differentiation, the sound being augmented in 
patency of the duct, absent in pulmonary stenosis. In case of doubt, 
the probability is altogether in favor of pulmonic stenosis, as much the 
more common lesion. 

Prognosis. — Congenital lesions of the heart are nearly always fatal 
in early life. Pulmonary stenosis may, however, permit the patient to 
reach adult life, and instances of survival to the age of forty-five years 
are on record. 

VII. TRICUSPID INSUFFICIENCY 

Incompetency of the tricuspid valve from local endocarditis is 
extremely rare, while it naturally results (1) from dilatation of the 
right ventricle in the terminal stages of left-sided lesions of the heart, 
or (2) from obstruction to the pulmonary circulation due to emphy- 
sema, chronic interstitial pneumonia, advanced tuberculosis, and the like. 

Symptoms. — Deep congestion of all the organs of the body and 
anasarca, as seen in the late stages of cardiac failure, are characteristic. 
These symptoms are superimposed upon those of the primary condition. 

Physical Signs. — Inspection. — Bulging of the precordial area, pul- 
sation in the epigastrium and the deep cyanosis, especially of the face 
and neck, are noticeable. General anasarca is usually present. 

As with each systole of the ventricle blood is driven back into the 
auricle and thence into the unguarded veins of the neck, a distinct 
venous pulse may be seen, especially in the right external jugular, some- 
times the left. 

Palpation. — The pulsation of the right ventricle in the precordium 
and the epigastrium may be notable. The most important signs to the 
touch are, however, the venous pulse in the neck, and a systolic jiulsa- 
tion of the liver edge, explainable on the like regurgitation of blood 
into the hepatic veins. 

Percussion. — The cardiac dulness is extended to a varying degree 
to the right of the sternum. 



DISEASES OF THE HEART 



201 



Auscultation. — A blowing systolic murmur resembling that of mitral 
insufficiency is heard over the lower portion of the sternum or in the 
4th or 5th spaces on either side close to it. 

Diagnosis. — The murmur of tricuspid insufficiency can be safely 
distinguished from that of a mitral insufficiency only by the accompany- 
ing signs. The location of the murmur is suggestive only. 

VIII. TRICUSPID STENOSIS 

Narrowing of the tricuspid orifice is too rare to be of practical 
importance. It has been found both as a congenital and an acquired 
lesion combined with some other defect. Of the latter class, 75 per 
cent, are in women and rheumatic fever is the usual cause. 

The SYMPTOMS are practically those of tricuspid insufficiency. Poly- 
cythemia is regularly found. The physicat. signs may be inferred. The 
presystolic murmur is heard over the lower sternum or even to the 
right of it. A presystolic thrill may be felt in the same situation. 

Diagnosis. — The lesion is difficult to distinguish from mitral 
stenosis or from tricuspid insufficiency. 

COMBI.VED VALVULAR LESIONS OF THE HEART 

The valvular lesions, described separately for the sake of simplicity 
and clearness, may be combined in all possible ways. (1) Lesions of 
the left heart greatly preponderate over those of the right. (2) Both 
mitral and aortic valves are often affected, and either valve may present 
the lesions of stenosis and insufficiency as well. (3) Aortic insufficiency 
or stenosis is more often combined with mitral insufficiency than with 
mitral stenosis. (4) Tricuspid lesions are more often associated with 
mitral than with aortic lesions. In the combined forms one lesion often 
dominates the clinical picture, the others being accessory only; on the 
other hand, the effects of one lesion may to some extent neutralize that 
of another. Thus mitral insufficiency with aortic insufficiency or ste- 
nosis partially relieves the strain upon the left ventricle, allowing part 
of it to fall upon the auricle. 

Sequelae and Complications of Chronic Endocarditis. — 1. In the 
Heart Itself. — (1) Dilatation and hypertrophy have already been 
described. (2) Myocarditis of some degree is frequently associated. 

(3) Acute pericarditis, with fibrinous or serous effusion, is a common 
complication in severe or advanced cases, and always a dangerous one. 

(4) Changes in the rapidity and rhythm of the heart action are fre- 
quent, (a) Regularly the heart action is rapid, occasionally so rapid 
as to warrant the designation of tachycardia — even 200 or more to the 
minute, (b) Bradycardia, on the other hand, is very unusual. It occurs 
at times in aortic stenosis, (c) Arrhythmia is very common, especially 
in mitral lesions. (See page 105.) While in most instances irregularity 
of the pulse is of serous import, there are many cases in which c()inp(>n- 
sation is thoroughly maintained with marked irreguhn-ity and intennit- 
tence of the pulse. 



202 



DISEASES OF THE CIRCULATORY SYSTEM 



2. Embolism. — In chronic endocarditis thrombi may easily form 
upon the valves themselves or on the adjacent endocardium, or by rea- 
son of the impaired circulation in the distal veins. From any of these 
sites small or large clots may be swept into the blood stream and lodged 
in any of the distal arteries of the body, such as, — (a) Cerebral. Apo- 
plectic attacks and hemiplegia follow, (b) Pulmonary, giving rise to 
hemoptysis and other signs of infarction, (c) Splenic, causing pain, 
tenderness and enlargement of the organ, (d) Renal, with pain and 
hematuria, (e) Femoral or brachial, leading to gangrene. 

3. Nervous Complications. — Embolism of the cerebral arteries has 
already been mentioned. Cerebral hemorrhage may occur. Apart from 
these definite organic lesions, serious mental disturbance is not uncom- 
mon in advanced valvular lesions. Melancholia is the more common 
type, but mild delirium or maniacal excitement may develop. 

4. Nutrition shows little change during the early stages, but late in 
the disease the patients regularly lose flesh and strength. The emacia- 
tion is often concealed for a time by edema, and appears more pro- 
nounced as the patient recovers and the edema lessens. 

5. Fever is present during the exacerbations of the endocarditis. The 
fever may be either constant or intermittent, high or low. 

6. Joint Symptoms. — As rheumatic fever is the cause of most cases 
of chronic endocarditis, stiffness and pain about the joints, either with 
or without redness and swelling, are frequently complained of. 

Prognosis. — The outlook in chronic endocarditis depends upon many 
factors. 

1. The Location and Nature of the Defect. — Any valvular lesion 
may be perfectly compensated and may remain so indefinitely. The 
mitral lesions are relatively more dangerous than the aortic, because 
the strain falls directly on the thin-walled auricle; especially is this 
true of mitral stenosis. Stenosis is in general more harmful than in- 
sufficiency. Multiple lesions complicate prognosis, because in some 
instances they add to the gravity of the condition, while in others one 
lesion offsets another and the combination is better borne than a single 
lesion. 

2. The Age of the Patient. — Endocardial lesions in childhood are 
relatively grave. They are in great part rheumatic; the disease tends 
to recurrences with aggravation of the endocarditis; it is almost impos- 
sible to prevent children from overtaxing weakened hearts in play or 
ordinary exertion. Their liability to acute infectious diseases increases 
the danger. 

3. Occupation. — Freedom from hard physical labor or severe ex- 
ertion is necessary to safety. Endocarditis is therefore more serious 
in men than in women, and especially among those whose occupation 
involves hard work. 

4. Temperament. — A calm and even mind is as important as ]^hysical 
(|Hi('t. Freedom from worry or excitement is quite as necessary as 
freedom from physical strain. 



DISEASES OF THE HEART 



203 



5. Condition of Arteries and Kidneys. — The presence of lesions of 
the arteries or kidneys always adds to the gravity of prognosis. 

Treatment. — 1. Prevention. — Inasmuch as chronic endocarditis 
results from acute infectious diseases, especially rheumatic fever or 
from the group of influences producing arteriosclerosis, such as alcohol, 
syphilis, lead poisoning, and gout, prevention must look to the reduction 
of infectious diseases and freedom from the toxic influences of the sec- 
ond group. The prevention of attacks of rheumatic fever, since this one 
disease accounts for more than 50 per cent, of all cases (see page 187), 
is therefore of prime importance. It is generally agreed that treatment, 
either by salicylates or alkalies, after the onset of an attack has little 
or no influence upon the frequency and severity of endocardial 
involvements. 

2. (a) During Compensation. — Avoidance of the influences likely 
to cause breaking of compensation (see page 191) is the prime consid- 
eration. A quiet, well-regulated life is called fqr, with strict observ- 
ance of the rules of hygiene and health. The diet should be simple 
and adapted to the digestive capacities of the patient. The reg- 
ular action of the bowels must be secured. Exercise must be 
adapted to the age and condition. Walking,- bicycle riding on level 
roads, golf and such like amusements should be encouraged. Any ex- 
ertion causing dyspnea or pain and palpitation should be avoided. 
Abundant sleep is a safe-guard. The use of alcohol or tobacco had best 
be forbidden and indulgence in tea or coffee carefully limited. Any 
intercurrent acute illness must be treated with care lest the established 
compensation be thereby impaired or broken. Medicines should be 
employed only for distinct indications, such as constipation, and cardiac 
stimulants are not called for. 

(b) In Broken Compensation. — Treatment must be influenced 
largely by the degree of disturbance and its cause. The milder mani- 
festations may be met by a limited reduction in mental and physical 
activity — without anything else. Indeed, many patients, especially the 
young and vigorous, even when evidences of serious disturbance have 
developed, promptly recover compensation when put to bed and reason- 
ably dieted, without the use of cardiac remedies. 

1. Rest, both physical and mental, is therefore the prime considera- 
tion. It must be graded according to the severity of symptoms. 
Usually rest in bed is most effective. In some of the severest cases, 
however, rest in bed is difficult or impossible, on account of orthopnea. 
The patient should then be made as comfortable as possible in an arm 
chair. Whatever contributes to comfort aids recovery. Peace of mind 
is as important as rest of body. 

2. The diet must be suited to the condition of the patient. In gen- 
eral it must be limited in quantity and easily digestible. Distention of 
the stomach from any cause adds greatly to dyspnea and distress. In 
severe cases fluids alone can be given, and milk in some form or modifi- 
cation is most often successful. In the presence of marked edema or 



204 



DISEASES OF THE CIRCULATORY SYSTEM 



anasarca the total amount of fluid given in twenty-four hours must be 
limited, and the use of salt restricted. 

3. The bowels should, as a rule, be moved daily, either by laxatives 
or enemata. If edema is present, saline laxatives to produce copious 
watery discharges are indicated. 

Medicines. — Digitalis in some form is regularly given for this con- 
dition. Theoretically some have argued that digitalis is contra-indi- 
cated, and likely to prove harmful in aortic insufficiency, because by 
slowing the heart rate it prolongs the period of diastole and therefore 
the reflux of blood into the left ventricle. Practically, however, trial 
is regularly made of digitalis even in this condition. The tincture in 
doses of v-xx minims every three or four hours, or the fresh infusion, 
3ij-iv. Care must be taken to be sure of the freshness and potency of 
the preparations. Failure often results from lack of care in these 
respects. If digitalis fails or is not well tolerated by the stomach, other 
remedies may be tried: — Tincture of strophanthus in doses of v-x 
minims. Caffeine, 3 to 5 grains. Strj^chnine sulphate, gr. 1/30-1/20, or 
spartein sulphate, 1 to 2 grains. The double salts of caffeine, caffeine 
sodium salicylate or caffeine sodium benzoate ma^^ be used hypoder- 
matically, in doses of from 1 to 5 grains. 

The diuretic effect of digitalis may often be increased by the ad- 
ministration of theocin, 2 to 3 grains, thrice daily. 

Within the last few years the use of a crystalline strophanthin 
intravenously has been recommended as a substitute for digitalis in these 
conditions. The remedy is given in doses of 1/120-1/160 gr. daily by 
injection into the median basilic or cephalic veins. Only one or two 
doses are ordinarily administered. The effect is continued by the ad- 
ministration of digitalis. If digitalis has already been given, the intra- 
venous injection of strophanthin may produce serious disturbance from 
heart-block. (See p. 220.) Remarkable results have at times been 
obtained from its use. 

Treatment of Special Symptoms. — 1. Pain or Palpitation. — :Mor- 
phine or opium may be used for the relief of severe pain or distress. 
The quiet and comfort obtained are often invaluable. An ice-cap may 
be kept continuously applied over the heart. Aconite may be cautiously 
used. 

2. Dyspnea. — If due to pain it may be relieved by morphine. If 
caused only by congestion we must rely upon stimulation of the heart. 
Cupping the chest or the practice of deep breathing may be helpful. 
If hydrothorax be present, the fluid must be aspirated. If large 
amounts of fluid are present, it is best to withdraw only 500 c.c. at a 
time, lest the sudden relief of pressure lead to fatal edema of the lung. 

If edema of the lungs occur we must rely upon cupping, the use 
of rapid stimulants such as nitroglycerine, camphor, caffein, and adren- 
alin, any or all of these to be used hypodermatically. 

3. 7\nasarca. — Digitalis and other diuretics, such as theocin, caffeine, 
diuretin, are indicated. Diuretin may be given in dosses of 10 grains 



DISEASES OF THE HEART 205 

three or four times daily — the others as indicated above. Free purgation 
with limitation of total fluids to one or two pints and the restriction of 
salt (salt-free diet) are reasonable measures. The saline purgatives or 
purgative mineral waters may be given before breakfast in doses sulfi- 
cient to cause free, watery movements. 

The feet and legs, if much swollen, should be kept elevated. Ban- 
daging or light massage is helpful. In extreme conditions free incisions 
through the skin of the leg, each several inches in length, may be made 
to produce free drainage. Southey's tubes for this purpose seem unnec- 
essary. Care must be taken to maintain asepsis in these procedures. 

4. Digestive Disturbances. — Vomiting may be persistent. If digi- 
talis is being given it must be stopped or given by rectum. Feeding 
should also be suspended and the stomach given a rest for 12 or 24 
hours, only sips of water being allowed. Then feeding may be gradu- 
ally resumed by giving milk or broth in small quantities, half an ounce 
once an hour or half hour, and gradually increasing. Delafield's mixture 
of equal parts of cream, milk and water, with cerium oxalate, 10 grains, 
and sodium bicarbonate 30 grains to every 6 ounces, is often well borne 
under these conditions. Egg albumin water and the like may be tried. 

Constipation in the early stages must be treated by giving laxative 
foods and fruits if possible, using the" simple laxatives, such as cascara 
sagrada, compound licorice powder, aloin, podophyllin, and the like. 
When edema is present, the saline laxatives are preferable. When the 
stomach is irritable, enemata must be relied upon. 

5. Insomnia. — The simple hypnotics, sodium bromide, trional or 
veronal, may be tried. Codeine or morphine may be added in small doses. 
As compensation is restored, the insomnia disappears. 

Physical Methods in the Treatment of Chronic Endocarditis. — Of 
recent years there has been a remarkable development of physical 
methods for the treatment of broken compensation. These methods are 
in general applicable only to the milder degrees of disturbance, marked 
by little or no edema, such as permit the patient to be up and about, or 
to the stage of convalescence, when edema has disappeared and the 
patient is able to be out of bed. 

I. Nauheim Bath s. — In the village of Nauheim, Germany, the 
waters of a number of springs containing much CO^, calcium chloride 
and sodium chloride, have for many years been used in the treatment 
of these conditions with such success that the baths are now produced 
artificially and used the world over. To what the baths owe their 
effects, the warm water, the gas (CO.) or the salts, or to their peculiar 
combination, is still an open question. At Nauheim waters which have 
lost part of their CO^, and some of the contained mineral matter by 
ebullition and deposition are first used, later the waters as they rise 
fully charged from the springs. A gradual increase in the amounts of 
gas and salts is thus secured nnd at the same time the influence of the 
bath is augmented by lowering the temperature. Artificial ])aths repre- 
senting as nearly as possible the natural waters are now used. 



206 



DISEASES OF THE CIRCULATORY SYSTEM 



1. Weak Bath. — To 10 gallons of water at 95° F. add one pound 
sodium chloride, II/2 oz. calcium chloride ; increase until 3 pounds 
sodium chloride and 41/2 ounces calcium chloride are used. Duration 
of bath 5 to 15 minutes; temperature 95° to 90°. 

2. Strong Bath. — To 10 gallons of water add sodiam chloride 3 
pounds, calcium chloride 414 ounces, and (to develop the COo) sodium 
bicarbonate 2 ounces, and 3 ounces hydrochloric acid, increasing to 8 
ounces alkali and 12 ounces acid. These chemicals are now supplied 
in appropriate packages hy all large drug firms. Duration and tem- 
perature of baths varied as above. 

II. Exercises. — (1) Swedish Movements. — A carefully gradu- 
ated series of muscular movements, at first entirely passive, later active 
and gently opposed by the operator. The movements begin with the 
simplest, finger flexion and extension, and progress through wrist and 
elbow to the shoulder, and then in like manner go over the lower ex- 
tremity. In this manner the duration and power of the exercises are 
slowly increased. 

(2) Zander Apparatus. — IMachines, driven by steam or electric 
power, have been contrived to accomplish all these movements for the 
patient (passive movements) and are in use in some large cities, and 
in centers for the treatment of cardiac diseases. 

(3) Schott Movements. — These are merely a series of graded exer- 
cises on the Swedish principle embodied in a system employed by Aug. 
and Th. Schott, of Nauheim, as an adjunct to the baths. Beginning 
^^dth the simplest movements of fingers, hands and arms, without resist- 
ance, the exercises progress to complicated movements resisted by an 
attendant. 

(4) Oertel Method (hill climbing). — The same principle of gradu- 
ated exercise is employed in a different manner. The patient is directed 
to dail}^ walk increasing distances up increasing grades, from 0° to 5°, 
5°-10°, 10°-15° and 15°-20°. At certain resorts, such as Hot Springs, 
Va., paths are laid out on this principle, with, distances and grades 
marked. 

IIECHANICAL AIDS IN THE STUDY OF THE CIRCLXATION 

Sphygmomanometer. — Within recent years various instruments 
designed to measure in terms of a column of water or mercury the 
pressure within the arteries have been brought into use. ]\Iany forms 
are now employed. The two in common use in hospital work are the 
Janeway and Stanton instruments (see Fig. 36). 

Either of these has three essential parts: (1) The cuff lined by a 
pneumatic bag or pouch, in which the air-pressure is raised. (2) A 
cautery bulb (Stanton) or Pollitzer bag (Janeway) for inflating the 
cuff. (3) The manometer with its scale. In using these instruments 
the cuff is fastened closel.y about the arm, as in the illustration, the cuff 
inflated till the pressure within it obliterates the radial pulse, then 
by means of a valve the pressure is allowed to fall till the pulse is again 



DISEASES OF THE HEART 



207 



felt and the reading of the manometer is taken at this point. This is 
the maximum or systolic blood-pressure. Many factors tend to make 
the method inaccurate, especially the varying thickness of the arm, and 
the varying thickness and resistance of the arteries. There are also 
many transitory influences, such as the taking of food, exercise, and 
respiration, to cause variations in the measurements. Nevertheless the 
sphygmomanometer measures the blood-pressure much more accurately 
than the finger, and records of the blood-pressure are now essential in 
the study of circulatory disturbances. 




Fig. 36 — Janeway sphygmomanometer, attached to arm, showing method of retention of cuff 
and arrangement of manometer, with PoUitzer bag inflator. 

The Orthodiagram. — Taking advantage of the power of the Roent- 
gen rays to penetrate the thorax and display the cardiac outline by its 
shadow, Franz M. Grodel, of Nauheim, has perfected an apparatus by 
which an accurate projection of the cardiac outlines is made. Much 
valuable information has thus been obtained of the size and shape of 
the heart under different conditions. The apparatus is, however, 
cumbrous and expensive, and involves such exposure of the operator to 
the rays that its use has thus far been very limited. 

The Roentgen Rays. — Either by the fluoroscope or by plates the 
form and size of the heart may be studied. The fluoroscope is objection- 
able, because of the exposure of the examin(M'. Skiagraphic phites are 
valuable, but their use has })een limited by the ei-rors in projection due 
to varying distances of plate, heart, and Roentgen tube. The heart 



208 DISEASES OF THE CIRCULATORY SYSTEM 



shadow cannot be taken to represent accurately the size of the organ, 
unless the tube is at such distance as to render the rays parallel and 
perpendicular to the plane of the plate. Efforts to secure such results 
by placing the tube at a distance of 8 feet or more are now being made. 
Even without attention to these points the skiagraphic plates are em- 
ployed to give a fairly accurate picture of the heart. 

HYPEETROPHY OF THE HEART 

Definition. — A thickening of the walls of one or more chambers of 
the heart. Hypertrophy^ may occur without other changes in the heart 
(simple hypertrophy^ ; it is usually accompanied by enlargement in 
the capacity of the affected chamber (hypertrophy and dilatation or 
eccentric hypertrophy) ; very rarely it occurs with normal content or 
apparent reduction in the size of the chamber (concentric hypertrophy, 
probably only apparent and explained by systolic contraction of the 
affected part). 

In the great majority of cases hypertrophy and dilatation, as pointed 
out in the last chapter, are the processes of adjustment by which com- 
pensation is brought about in chronic endocarditis, in myocarditis and 
adherent pericardium, and they present themselves not as independent 
conditions, but as attendant features of these diseases. In some cases, 
however, hypertrophy and dilatation occur independently of these dis- 
eases and indeed of one another, and for the sake of clearness it is 
necessary to study them separately. 

Etiology. — The cause of hypertrophy in the heart muscle, as in any 
other striped muscle, is overwork. The hypertrophy appears particu- 
larly in the thick-walled ventricles, and in left or right according to 
the location of the strain. The auricles are less often and less strik- 
ingly affected. Not infrequently all the chambers are involved. 

Hypertrophy of the left ventricle may result from (1) Excessive 
muscular exercises. Athletes, race-horses, and the like, regularly have 
hearts larger than the average, yet the degree of hypertrophy thus 
caused is moderate. (2) From heart lesions, such as aortic stenosis 
or insufficienc3\ or mitral insufficiency, chronic myocarditis, pericardial 
adhesions. (3) From overactivity or palpitation due to excessive thy- 
roid secretion (exophthalmic goitre), the persistent use of alcohol, tea, 
coffee or tobacco, and the like. (4) From increased arterial tension, 
due to arteriosclerosis. Bright 's disease, and the like. 

Hypertrophy of the right ventricle may result from (1) ]\Iitral 
lesions or remotely aortic lesions. (2) Pulmonary valve lesions (rarely). 
(3) Obstruction to the pulmonary circulation, such as occurs in emphy- 
sema or interstitial pneumonia or tuberculosis. (4) Pericardial adhesions. 

Hypertrophy of the auricle on the left side is due to stenosis or 
incompetency of the mitral, on the right to like conditions of the 
tricuspid valve. 

Morbid Anatomy. — For the most part the lesions are those of the 
underlying conditicms. In the heart itself the Avail of one or another 



DISEASES OF THE HEART 



209 



chamber is thickened, especially of the ventricles. The greatest hyper- 
trophy is seen in the left ventricle, which may be two or three times its 
normal thickness. The size and weight of the whole heart is increased. 

Symptoms. — Under ordinary conditions there are no symptoms, the 
condition being compensatory. If symptoms do appear, these are more 
likely to result from the underlying cause of the hypertrophy than from 
the hypertrophy itself. Precordial uneasiness, or discomfort, or palpi- 
tation, sometimes insomnia, may possibly be due to hypertrophy alone. 

HYPERTROPHY OF THE LEFT VENTRICLE 

Physical Signs. — Inspection. — Prominence of the precordium, espe- 
cially in children. Apex displaced downward and outward, in sixth or 
seventh interspace. Impulse forcible, possibly heaving and wide. Pal- 
pation confirms the location and character of the impulse. Percussion 
shows the enlargement in the area of deep dulness, to the left. Aus- 
cultation. — The first sound is low-pitched and prolonged, the second 
aortic sound accentuated or reduplicated. 

Hypertrophy of the right ventricle gives rise to prominence of 
the lower sternal region in children, an epigastric pulsation, and ac- 
centuation of the second pulmonic sound. 

The pulse is not materially modified unless it be by the influences 
producing the hypertrophy. 

Radiographic examination shows the increase in the size of the 
ventricles, either right or left, and also, indeed, of the auricles. It is 
especially valuable in cases of emphysema, where the distention of the 
lungs obscures the normal heart dulness. 

Diagnosis. — From nervous palpitation, the condition may be dis- 
tinguished by accurately determining the size of the heart. Unusual 
exposure of the heart due to retraction of the lung and caused by 
chronic pleurisy or interstitial pneumonia may confuse one. Here 
again the exact determination of the size of the heart is important. 
The sounds also are normal. Particular care is necessary in emphysema. 

Prognosis depends entirely upon the cause and upon any signs of 
dilatation. 

Treatment. — During compensation, treatment must be wholly di- 
rected to the cause of the condition and the avoidance of any causes of 
disturbance (see p. 191). When compensation fails the treatment is 
that of broken compensation. 

DILATATION OF THE HEART 
Definition. — Enlargement of one or more of the chambers of the 
heart. If previously normal the walls become thin ; if hypertrophied, 
they may remain thick or appear of normal thickness. Hypertrophy 
and dilatation are usually associated. 

Etiology. — The causes of dilatation may be grouped under two 
heads: (a) weakening of the walls of the heart, or (b) increase of 
pressure within the heart (see Rupture of Compensation, p. 191). 
14 



210 DISEASES OF THE CIRCULATORY SYSTEM 



Usually the two factors are combined. Dilatation tends of itself to 
increase. The larger any chamber of the heart becomes, the more blood 
it holds, the heavier its work, and therefore the greater the strain put 
upon it. 

Morbid Anatomy. — Any or all the chambers of the heart may be 
enlarged. Usually there is more or less hypertrophy accompanying the 
dilatation. If the ventricles are dilated^ the mitral and tricuspid valves 
become relatively incompetent, rarely the aortic or pulmonary. The 
endocardium is opaque and the myocardium regularly shows more or 
less marked degenerative changes. Arteriosclerosis and chronic Bright 's 
disease are commonly present. 

Symptoms. — As already pointed out, dilatation and hypertrophy are 
the protective measures by which the heart meets defects such as those 
of chronic endocarditis, myocarditis, arteriosclerosis, etc. In the early 
stages, therefore, dilatation produces no symptoms, but rather prevents 
those consequences which might otherwise follow valvular or other 
defects. In time, however, dilatation reaches the point where the cir- 
culation can no longer be properly maintained and signs of cardiac dis- 
tress and progressive venous stagnation appear. The sjnnptoms are 
therefore those given under rupture of compensation. In acute dilata- 
tion such as occurs during some of the acute infectious diseases the 
symptoms develop suddenly, it may be in a moment. Usually they are 
gradually evolved, covering some weeks of increasing distress. 

Once dilatation has occurred the prospect of re-establishing com- 
pensation depends largely upon the cause of the dilatation and the part 
of the heart involved, the ventricles much more readilj^ than the auricles 
recovering power. 

Usually, as indicated under valvular lesions, compensation is re- 
stored and the patient lives for a varying length of time, till condi- 
tions again arise disturbing compensation. The picture of cardiac 
failure then develops ancAv. Such recurrent attacks are likely to end 
in one too severe to be recovered from. 

Physical Signs. — Inspection shows a diffuse but feeble pulsation, 
or none at all. The apex impulse is faint or indiscernible. Evidences 
of hypertrophy may be seen in the prominence of the precordium. Pal- 
pation confirms these findings. Percussion gives a great increase in the 
area of cardiac dulness either to left or right or both, depending upon 
which chambers are involved. The area of cardiac dulness is still of 
normal form and the acute cardiohepatic angle is preserved. 

Auscultation discloses the murmurs of mitral, and possibly tricuspid 
insufficiency. These may be accompanied by pre-existing aortic mur- 
murs. If the heart's action is very feeble, there may be no audible mur- 
murs and the heart sounds may be so faint as to be heard with difficulty. 

The pulse is rapid, small, weak and probably irregular and inter- 
mittent. The patient gives all the other signs of cardiac failure — 
cyanosis, edema, ascites or hydrothorax, enlarged spleen, palpable and 
possibly pulsating liver. 



DISEASES OF THE HEART 



211 



Diagnosis. — Pericarditis with effusion presents a clinical picture 
distinguishable in some cases only with difficulty. A knowledge of the 
previous condition of the patient, or the fact that a dry pericarditis is 
known to have preceded the condition, is of the utmost value. The 
shape of the area of cardiac dulness in pericarditis with effusion is 
different from that of an enlarged heart, being much broader along the 
diaphragm, and the cardiohepatic angle can usually be demonstrated as 
normal in dilatation. The heart sounds and cardiac murmurs are more 
likely to be heard in dilatation than through a large pericardial effusion. 
The increased cardiac dulness in pericarditis, if studied carefully at 
intervals, is found to be progressive, while that in dilatation is more 
likely to remain fixed. 

In severe infectious diseases such as typhoid fever, pneumonia, or 
sepsis, circulatory failure marked by cyanosis, a rapid, small, weak 
pulse, profound prostration, possibly pulmonary edema, and often ter- 
minating in death, is common. Such circulatory failure has long been 
attributed to failure of the heart assumed to be due to weakening of the 
heart muscle and dilatation of the heart. 

Careful study in many such cases, however, shows that there is no 
increase in the cardiac dulness, that the heart sounds are clear and dis- 
tinct, and that the apex impulse is definite, possibly forcible. Experi- 
mentally it has, moreover, been sho^vn that this circulatory failure is 
due to vasomotor paralysis, especially of the splanchnic vessels, and not 
to ''heart failure." The distinction is important with reference to 
treatment. Such vasomotor paralysis is to be met, not by digitalis or 
other heart stimulants of that class, but by cold applications to the 
abdomen (ice-coil or ice-bag) and the administration of caffeine, 
camphor or adrenalin, or clyses of normal salt solution. 

Treatment is that given for broken compensation (see p. 203). 

DISEASES OF THE MYOCARDIUM 

MYOCARDITIS 

(Myocardial Degeneration. Infarction of the Heart. Sclerosis of the Heart) 

No subject in internal medicine is fraught with greater difficulty 
than that of the pathology and symptomatology of disease of the heart 
muscle. The lesions found differ markedly from those common in other 
organs and many times are of the type of degeneration rather than 
inflammation. They frequently appear in patients who have presented 
no evidences of cardiac disturbance ; they are often lacking when con- 
fidently expected. The diagnosis of myocarditis is thus always attended 
with some degree of uncertainty. 

Frequency. — IMyocardial lesions are much more common than is sup- 
posed. In the study of the heart the more obtrusive lesions of the valves 
and pericardium long received more attention. Most cases of disease 
of either endo- or pericardium are accompanied by lesions of the muscle 



212 DISEASES OF THE CIRCULATORY SYSTEM 



and as English writers have pointed out the condition is neither endo- 
carditis nor pericarditis, but a carditis, an inflammation of all the 
structures in the heart wall. 

But myocardial changes are present in many cases independently 
of disease of the endocardium or pericardium, especially in arterio- 
sclerosis with involvement of the coronary arteries. Acute degenera- 
tions of the myocardium are also caused by the influence of many infec- 
tions and toxemias. On the whole, therefore, myocarditis is a fre- 
quent finding in post-mortem w^ork and is doubtless present in many 
cases in which hitherto it has been unthought of. 

ACUTE MYOCARDITIS 

Etiology. — (1) Acute infections are the most common causes, espe- 
cially diphtheria, typhoid fever, influenza and rheumatic fever. (2) 
Pyemia, gonorrhea and similar pyogenic infections may cause inter- 
stitial myocarditis from the lodgment of septic emboli in the heart 
muscle. (3) Embolism or thrombosis of the coronary artery, not in- 
fective, may cause acute degeneration (necrosis) of the heart muscle. 
(4) Certain severe toxemias, such as the toxemia of pregnancy or acute 
yellow atrophy, may cause myocardial changes. 

Morbid Anatomy. — The heart may be normal in size, or the muscle 
may feel unusually relaxed and soft, or the chambers, especially the 
left ventricle, may be dilated. The muscle may on section appear nor- 
mal, but usually ill-defined patches in Avhich it is paler, or more yel- 
lowish, and cloudy in appearance are found. These patches are most 
easily found in the walls of the ventricles. They are soft and easily 
torn. 

Microscopically the lesions found, although varying greatly, may 
be classified as parenchymatous or interstitial. The lesions of the 
muscle fibres proper are difficult to describe or to classify satisfactorily. 
Special methods of treatment and study are often necessary for their 
recognition. The muscle fibres may be swollen, stain poorly, be more 
granular than normal, show abundant fatty degeneration, or hyaline 
degeneration, or be broken in various ways. The interstitial tissue shows 
lesions varying from minute foci of infiltration with lymphoid and 
plasma cells to definite abscesses. Some degeneration of the neighboring 
muscle always accompanies these changes in the interstitial tissue. 

Symptoms. — These may develop during the course of an acute in- 
fection, such as diphtheria or influenza, or they may follow it. In 
severe cases syncope or sudden death may be the first symptom. In 
milder cases the patients are pale and prostrated "vvith great muscular 
relaxation, or, if able to be up, they complain of weakness and pain and 
palpitation on any exertion. 

Physical Signs. — The heart impulse is feeble, the sounds faint and 
the pulse is weak, rapid or irregular. In other cases the heart is dilated 
and there are murmurs of insufficiency over one or more valves. 

Prognosis. — The outlook is favorable when the condition is recog- 



DISEASES OF THE HEART 



213 



nized and properly treated. The possibility of sudden death, especially 
after diphtheria, must be borne in mind. 

Treatment. — The early treatment of diphtheria by antitoxin is to 
some extent preventive. Rest, limited or absolute, according to the 
severity of the condition, is essential and must continue till all symp- 
toms disappear. 

Gastric distention must be avoided by careful and restricted feed- 
ings. Strychnine, camphor, Caffein, may be used hypodermatically, if 
necessary. Digitalis is to be avoided. 

CHRONIC MYOCARDITIS 

Etiology. — Chronic myocarditis is in most cases an accompaniment 
of disease of the coronary arteries, chronic endocarditis or pericarditis. 
It may therefore have the causation of any of these conditions. It is. 
peculiarly closely related to disease of the coronary arteries and etiolog- 
ically to arteriosclerosis in general. Emphasis should be put upon the 
importance of syphilis, gout, alcohol, and age. 

Chronic myocarditis is therefore a disease of adult life, and espe- 
cially of men. 

Morbid Anatomy. — The heart regularly shows dilatation and 
hypertrophy in some degree. Chronic endocarditis or pericarditis, or 
atheroma of the aorta and sclerosis of the coronaries are to be expected. 
The heart muscle is flabby, pale yellow or gray, more friable than nor- 
mal, either in patches or diffusely. 

Microscopically the interstitial tissue is thickened and increased 
and infiltrated with small round cells. The muscle fibres are more or 
less degenerated and replaced by fibrous tissue. 

The changes in the coronary arteries are of such importance that 
they deserve special mention. The arteries show the usual changes of 
arteriosclerosis, thickening of the wall, tortuosity, degeneration of the 
intima and changes in the calibre of the vessel. Not infrequently the 
lumen of one of the branches is blocked by a thrombus or an embolus. 
If the circulation is only impaired, fibrosis occurs. If it is entirely 
shut off, necrosis may result. 

We must include under the heading of Chronic Myocarditis the 
condition of fatty heart, although it is not inflammatory but degen- 
erative in nature. 

Fatty Heart. — Two forms of this condition are recognized: (1) 
Fatty degeneration, the muscle fibers showing degenerative changes with 
abnormal fatty deposition. This condition may result from a varietj^ 
of conditions: (a) Failing nutrition from old age or cachectic states, 
(b) In protracted infectious fevers, (c) Pernicious anemia or phos- 
phorus poisoning, (d) Chronic affections of the endocardium or peri- 
cardium or of the heart muscle itself, as in dilatation and hypertrophy. 

(2) Fatty overgrowth. In obese persons an excessive deposit of fat 
is regularly found under the pericardium, sometimes almost concealing 
the heart muscle. In certain instances the fat not only overlies the 



214 DISEASES OF THE CIRCULATORY SYSTEM 



muscle, but penetrates into it, displacing the muscle strands and appar- 
ently replacing them. The muscle fibers may disappear and the 
ventricular wall show little but fat. 

Symptoms. — Clinically the cases of chronic myocarditis may be 
grouped under three heads : 

1. Sudden Death. — ^Myocarditis is the most frequent cause of sudden 
death due to internal disease. And in these cases thrombosis or em- 
bolism of the coronary arterj^ is the common finding. 

2. Failure of compensation in chronic endocarditis or in arterio- 
sclerosis is often dependent upon myocarditis. These cases present 
themselves with sjTiiptoms of broken compensation, dyspnea, cyanosis, 
edema, etc., and signs of dilatation of the heart and run the course 
described under broken compensation. 

3. Cases with weak, irregular heart action, often slow, and evidences 
of incompetency of the heart, such as feebleness or prostration, dyspnea 
on exertion, pain and palpitation and sjTicopal attacks or epileptiform 
convulsions, the so-called Stokes- Adams sjTidrome (see Arrh^i:hmia, p. 
224). These patients may continue to have difficulty and ultimately die 
in one of the attacks, or from dilatation with the usual signs of cardiac 
incompetency. 

Prognosis is always grave. The possibility of sudden death in any 
case must be borne in mind. Much depends upon the condition of the 
arteries and kidneys, still more upon the ability of the patient to lead 
the life of freedom from severe mental or bodily effort or anxiety caUed 
for. 

Treatment. — The treatment must be that of the underlying condi- 
tion (see Arteriosclerosis) or of failure of compensation if that condi- 
tion develops. 

NEUROSES OF THE HEART 
PALPITATION 

Definition. — Irregularity in the force or frequency of the heart 
action felt by the patient. Palpitation is usually associated with 
rapidity of the pulse, but may accompany a normal rate or even brady- 
cardia. 

Etiology. — 1. Palpitation is one of the early symptoms of failing 
compensation and may belong, therefore, to any of the organic lesions 
thus far considered. ' 

2. Palpitation may be a pure neurosis depending upon (a) neuras- 
thenia, (b) gastric diseases, especially the nervous disturbances of 
digestion, (c) the abuse of alcohol, tobacco, coffee, or tea, (d) sexual 
excesses and diseases of the uterus or ovaries. ^lenstraation is often 
accompanied by palpitation or it may come on at puberty or the meno- 
pause, (e) Exophthalmic goitre or excessive doses of thyroid extract. 

Symptoms. — The cardinal symptom is the consciousness of abnormal 
heart action. The heart action is exaggerated in force and either rapid 
or slow. The aorta, and the great arteries of the neck may throb vie- 



DISEASES OF THE HEART 



215 



lently. Manifold other symptoms due to the associated diseases (neuras- 
thenia, or valvular lesions, etc.) may be present. 

Physical Signs. — If organic disease of the heart is present the 
physical signs of such lesion will be found. In other cases the heart 
apex is located within normal limits, but the impulse is commonly over- 
forcible. The area of dulness is not increased. The heart sounds are 
rapid or slow, exaggerated in force, often functional murmurs are pres- 
ent at the base, sometimes at the apex. The increased pulsation of the 
aorta and great vessels is often striking, the pulsation of the aorta some- 
times suggesting aneurism. 

Prognosis is good both as to life and health. The duration must 
depend upon the underlying causes and the possibility of their removal. 
Recovery is usually prompt under proper treatment. 

Treatment. — Of first importance is the removal of the cause, espe- 
cially the prohibition of alcohol, tobacco, coifee and tea. This may in- 
clude the adequate treatment of gastric disturbances, neurasthenia, sex- 
ual disorders, organic disease of the heart or exophthalmic goitre. If 
the disturbance is limited to the heart alone it had best be treated on the 
principles of a neurasthenia. An out-door life, reasonable diet, mod- 
erate exercise and freedom from worry or anxiety, will, as a rule, 
promptly restore normal action. Bromide of soda, valerian, or asafetida 
is commonly given, but they are of value only as they affect the general 
nervous tone. 

Assurance given the patient of the absence of any organic disease 
of the heart or danger of death is of the utmost value. 

TACHYCARDIA 

Any increase in rate of the heart action may be termed tachycardia. 
As a rule this designation is employed only for the severer grades of 
disturbance, in which the rate varies from 120 to 200 or more. Palpi- 
tation and tachycardia are commonly associated. 

Etiology. — The causes are for the most part those of palpitation. 
Fever regularly gives rise to increase in the pulse rate. Fright may lead 
to persistent frequency. Lesions of the medulla or the pneumogastric 
nerve are found to explain some cases. 

Paroxysmal tachycardia is a rare affection marked by attacks of 
tachycardia with intervals of normal heart action. The pulse may 
attain a rate of 200 or more per minute. The attacks of rajnd action 
may last for minutes or days. They come without discoverable cause 
and cease as unaccountably. 

Treatment. — The cause must be sought for and if possible removed. 
(See Palpitation.) In the idiopathic cases, rest must be required. An 
ice-cap should be applied to the precordium. Tincture of aconite in 
doses of from 2 to 5 minims may be given every three or four hours, 
or digitalis may be tried, although it usually fails of effect. 



216 DISEASES OF THE CIRCULATORY SYSTEM 



BRADYCAKDIA— SLOW HEART 

In certain families a slow pulse may be normal. In some cases a 
rate near 40 to the minute persists throughout life. Care should be 
taken to be sure that all the heart beats are perceptible at the wrist. A 
person may have an infrequent radial pulse when the heart is beating 
rapidly through failure of part of the pulsations to reach the wrist. 

Bradycardia appears to be normal in some conditions such as old 
age, the puerperal state, or hunger. It is also seen in various other 
conditions, such as (a) the convalescence from acute fevers, especially 
pneumonia, typhoid fever, acute rheumatism and diphtheria. The pos- 
sible relation of myocardial degeneration to these conditions has been 
pointed out (see p. 212), but bradycardia often appears without other 
symptoms and passes off without consequence, (b) Diseases of the 
digestive system, chronic gastritis, ulcer or cancer of the stomach, 
chronic jaundice, (c) Diseases of the heart, especially myocarditis, of 
the fatty or fibrous type, (d) In uremia and in poisoning by lead, 
alcohol, tea, coffee or tobacco, (e) In anemia, chlorosis or diabetes, (f ) 
In increased intracranial tension from hemorrhage, tumor, increased 
cerebrospinal fluid or inflammatory exudation, (g) In a variety of 
other conditions, such as diseases of the skin or sexual organs. The 
treatment must be directed to the primary condition. 

ARRHYTHMIA 

Disturbances of the rhythm of the heart have of recent years received 
an unusual amount of attention by reason of interest aroused by new 
methods of study and new conceptions of cardiac physiology. The 
present views in this relation may be stated, as follows : — 

I. Myogenic Theory. — The heart muscle possesses a number of more 
or less interdependent functions — (1) contractility, (2) rhythmieity, 
(3) conductivity, (4) sensibility, (5) tonicity. According to these 
views the heart muscle possesses within itself certain powers which give 
rise to rhythmic contractions. These start in the auricles near the great 
veins and are transmitted to the ventricles and stimulate them to con- 
traction. Under normal conditions the rate of auricular contractions 
determines the rate of systole of the ventricles. The maintenance of 
these relations depends upon several factors, (a) The normal rhythm 
of auricular contractions. It has been established that the rhythmieity 
of the heart depends upon rhythmieity in sensibility to stimuli. In 
this regard the muscle shows alternating periods of sensibility and 
insensibility. The former includes the period from just before to just 
after contraction, the latter the remainder of each phase. A stimulus 
reaching the muscle in the sensitive periods causes a contraction, while 
in the refractory period no result follows. The even beat of the ventricle 
depends upon the mnintenanee of normal rhythm in the auricle, (b) 
ITpon the ready conduction of impulses from the auricle to the ventricle. 
The anatomist has shown that the only direct connection between auricles 
and ventricles is a minute band cf muscular fibers (bundle of His, see Fig. 



DISEASES OF THE HEART 



217 



37), arising in the auricular septum just beneath the foramen ovale, 
passing downward through the auriculo-ventricular septum, lying at 
this point just under the mesial leaflet of the tricuspid valve, into the 
interventricular septum and there breaking up into a cobweb of fine 
branches which are distributed to various parts of both ventricles and 
the papillary muscles. The integrity of this bundle is essential to the 
normal relation between auricular and ventricular contractions. 
Physiologists have demonstrated that if this path of transmission be 
impaired, the ventricle fails to answer to some of the auricular con- 
tractions (see Fig. 38). The failure may be partial, one in every four, 
three or two beats (partial heart-block), or it may be complete (complete 
heart-block). In the latter case auricle and ventricle are found beating 




Fig. 37. — The sinus region of the heart, the veno-auricular or veno-sinal bands of striated muscle 
and the auriculo(atrio)-ventricular or sinu-ventricular muscle bundle. (Schematic, constructed from 
the findings of Keith, Schonberg, and Retzer.) A. Seen from the right side. The dotted area repre- 
sents the sinus region; the striee represent the veno-auricular muscle strands. V. C. S., superior vena 
cava; V.C.I., inferior vena cava; SC, coronary sinus; AV B, auriculo(atrio)-ventricular muscle bundle 
(His bundle); TRIC, tricuspid valve; PAP, papillary muscle. B. The same region seen from the front. 
MIT, mitral valve; AO, aorta. (Herschfelder's Disea.se3 of the Heart.) 



rhythmically, but with rates independent of . one another, the auricular 
rhythm being about 60-72 to the minute, the ventricular 28 to 36, 
approximately one-half the auricular rate. (3) Upon normal sensibility 
to stimuli on the part of the ventricular muscle. 

Over this muscular mechanism of the heart the nervous system 
presides with its center in the medulla, its vagus and sympathetic nerves. 
By these agencies the heart is made to respond to nervous influences 
either originating in the medulla or reflected upon it from other parts 
of the system. Thus by nervous stimulation the rate of the heart may 
be slowed (vagus) or accelerated (sympathetic). 

II. Neurogenic Theory. — No such independence of the heart muscle 
is recognized, and the functions of the heart are attributed not to the 
powers of the heart muscle alone, but to the influence of certain nerve 
ganglia found in its walls. Thus the origin of the automatic stimuli is 



218 



DISEASES OF THE CIRCULATORY SYSTEM 



found in the ganglia of Remak at the junction of the great veins and 
the auricles and these stimuli are transmitted not through the bundle 
of His but through nerve-fibers, on which certain other ganglia of 
Biedert are found. 




Fig. 38. — Heart showing an ulcer of the septum invohang the bundle of His and proaucing complete 
heart-block. From the collection of Dr. Walter B. James. 

It is not possible to accept unreservedly either theory and the final 
truth Avill doubtless prove to be a combination of both. 

Methods of Examination. — Our understanding of cardiac arrh5i:h- 
mias has been greatly broadened by the introduction of new methods 
of study. 

1. The Sphygmograph. — From the crude apparatus with which 
curious little tracings of the radial pulse used to be made, we have 



DISEASES OF THE HEART 



219 



advanced to more or less complex and costly apparatus permitting 
tracings: (a) From the wrist (radial or brachial pulse), (b) From 
the neck, giving a combination of the pulse waves in the carotid artery 
and the jugular vein, (c) From the precordium, giving the contrac- 



Respiratort 

AliLORRHYTHMIA 



AURICULO- 

VENTRICULAR 
HEART-BLOCK 



Alternating 

PULSE 



ATTRICtTLAR 
extras YSTOLE 



Ventricular 
extras ystole 



auriculo- 
ventricular 
extras ystol e 



Perpetual 
arrhythmia 



Paroxysmal 
tachycardia 





Fig. 39. — Diagram representing various types of irregular pulse. The heavy white arrows 
indicate the site of origin of the disturbance of rhythm. The heavy white lines indicate the course of 
the abnormal cardiac impulses. REtil', respiration; AUR, auricle; A-F or AVB, auriculo-ventricular 
bundle; VENT, ventricle; CAR, carotid pulse; VEN, venous pulse; SIN, sinus region of the heart; 
SVC, IVC, superior and inferior venae cavae, respectively. (Hirschfelder's Diseases of the Heart.) 



220 DISEASES OF THE CIRCULATORY SYSTEM 



tion of left or right ventricle according to the adjustment, (d) From 
the esophagus in juxtaposition to the left auricle. 

Tracings from these several sources taken and compared enable one 
to follow quite accurately the sequence of events in the several chambers 
of the heart and determine their relations (see Fig. 39). 

The accompanying illustrations taken from Hirschf elder's " Dis- 
eases of the Heart and Aorta " illustrate tracings from the more im- 
portant types of arrhythmia. The tracings below the bars are from 
the carotid artery and show only the sharp rise representing ven- 
tricular systole and the slow fall. The tracings above the bars are 
more complicated, showing several waves, marked a, c, v. The a-wave 
is that produced by the auricular contraction and as can be seen by com- 
parison with the arterial tracing just precedes the ventricular systole. 
The c-wave is the carotid wave, that is, a wave in the vein correspond- 
ing to the wave in the carotid artery and synchronous with it. The 
meaning of the v-wave is not so clear, and authorities differ in its inter- 
pretation. Mackenzie explains it as due to the storing of blood in the 
auricle. The crest of the wave corresponds to the opening of the tri- 
cuspid valves. 

Respiratory Allorrhythmia.- — Quickening and slowing of the 
pulse occur with the phases of respiration, but each cardiac cycle is 
complete. 

Auriculo-Yentricular Heart -BijOCK. — Certain of the impulses 
arising in the auricle are prevented from reaching the ventricle. The 
corresponding auricular systoles are therefore not followed by ven- 
tricular systoles ; a-waves appear in the venous pulse with no subsequent 
rise in the arterial tracing. 

Alternating Pulse (Pulsus Alternans). — The systoles follow one 
another in regular sequence, one strong, the next weak. 

Auricular Extrasystole. — From time to time extrasystoles appear 
in the arterial tracings, each, however, preceded by an appropriate 
auricular systole, upon which the extrasystole depends. 

Yentricular Extrasystole. — In this form the extrasj^stole arises 
in the ventricle, and is followed by a retrograde auricular systole. 

Auricut:.o-Yentricular Extrasystole. — Here the impulse arises in 
tissue joining auricle and ventricle and stimulates both to contract at 
practically the same time instead of in the normal sequence. 

Perpetual Arrhythmia. — In this condition the auricles are said to 
be paralyzed, no a-waves appearing in the venous tracings and ■ the 
ventricular contractions following without order, but there is evidence 
to show that the auricles are not inactive, but that the auricular fibers 
instead of contracting together in a normal manner are acting rapidly 
in feeble groups, fluttering or fibrillating, like the fibrillary contrac- 
tions of voluntary muscle. Some of these imperfect contractions are 
strong enough to initiate responses in the ventricle, others are not, and 
the consequence is a ])ulse without rhythm either as to the sequence of 
the rises or their strength, the perpetually irregular pulse. 



DISEASES OF THE HEART 



221 



Paroxysmal Tachycardia. — Two quite distinct types of pulse are 
commonly included under this title. In one the cardiac cycle is normal 
and the contraction of the ventricle follows that of the auricle in the 
usual manner, but the rate of action is greatly quickened, and the pulse 
beats number 150 or even 200 per minute. Such cases are practically 
excessive palpitation. In the second type the rapid action is associated 
with irregularity of the pulse and is usually dependent upon fibrillation 
of the auricules. In these eases the pulse may quickly double its rate 
or as quickly drop back to the usual rhythm. 

2. The Electrocardiogram. — The so-called string-galvanometer of 
Einthoven, of Leyden, has recently played a considerable role in the 
study of the irregularities of the heart. The following explanation of 
the principles of the apparatus is taken from the article of Drs. W. B. 
James and H. B. Williams, Am. Jour. Med. Sc., Sept. and Nov., 1910. 

Whenever a current of electricity passes through a magnetic field 
at right angles to the lines of force, it tends to be deflected to one side 
or the other, according to its direction. If we stretch a conductor 
between the poles of a magnet at right angles to the lines of force, it 
will tend to be deflected when traversed by a current, the direction of 
the deflection depending upon the direction of the current. Einthoven 
constructed a powerful electromagnet, through the field of which he 
stretched a very delicate fiber, which was either a fine platinum wire 
or a quartz thread w^hich had been silvered to render it a conductor. 
The diameter of the finest strings measures as low as 2.5/a, or about ^^ 
the diameter of a red blood corpuscle, and they are invisible to the naked 
eye except in a strong light. The mass is so small that it is unweighable. 
A micrometer screw enables the operator to increase or diminish the 
tension of the string at will, and so vary the sensitiveness of the instru- 
ment. An arc light operating in connection with a system of condensing 
lenses, and an objective and projection ocular project the shadow of 
the string upon a screen, the varying of the distance of which enables 
one to secure any magnification that may be desired. 

By a simple apparatus, the movements of the shadow of the string 
on the screen are photographed on a moving film and this preserved for 
study. The curves resulting are found to vary with the points of appli- 
cation of the electrodes. Three standard adjustments of the electrodes 
or leads are now employed: 

I. Right arm and left arm. 
II. Right arm and left leg. 
III. Left arm and left leg. 

The normal record (see Fig. 40) is seen to present a base line 
which shows the position of the string when no current passes, that is, 
when the potential of its two ends is the same, and starting from the 
base line are five waves lettered P, 0, R, S, and T. The best understood 
and most important of these are those which rise above the base line, 
that is, which are positive, P, R, and T. The term positive here has 



222 DISEASES OF THE CmCULATORY SYSTEM 



Q3 . 



R 



ec. 




««« 

« 



LE^i5 IT 



T 



LEAD III 



^ Sec- 



Fig 40 —Electrocardiogram of a healthy adult male, taken while sleeping. (Am. Jour. Med. 
Sci., vol. 140, page 418.) 



DISEASES OF THE HEART 



223 



reference only to the direction of the curve with reference to the base 
line. Each of these positive waves means that the base of the heart is 
electrically negative to the apex, or, to be more exact, that the algebraic 
sum of all the differences of potential that exist in the heart at that in- 
stant results in negativity of the upper end of the string toward the 
lower end to an extent indicated by the amplitude of the wave. P corre- 
sponds to the contraction of the auricle. The causal relation between 
auricular systole and P has been positively established by study of the 
exposed heart in animals, as well as by the observation of cases of 
auriculo-ventricular dissociation in human beings. Q, R, S, and T all 
correspond to the systole of the two ventricles. R and T are the most 
constant of these, and, as far as our present understanding goes, are the 
most important and useful in electrocardiography. R and T are always 
present in health, while Q and S may, either one or both, be absent. 

Observers are not in entire agreement as to the significance of the 
waves that make up the ventricular portion of the curve, but the fol- 
lowing is a summary of the leading views : 

The space between P and Q indicates the time elapsing between 
excitation of the auricles and ventricles, and is, therefore, the best meas- 
ure we have of the auriculo-ventricular interval. 

Q directed downward, and therefore indicating negativity of the 
apex toward the base, has been supposed by Einthoven to be due to an 
initial contraction of apical fibers, and the variations in this wave in 
individual cases to be due to variations in the- distribution of the fibers 
of the bundle of His. Q in health is always small and is often absent. 
It passes at once into R, the highest, most uniform and useful of all 
the waves. 

R corresponds to the initial contraction of the ventricles at the base, 
and indicates marked negativity of the base of the heart. It is possible 
that it is produced by the initial contraction of the papillary muscle 
system. As has been shown by Hering, the papillary muscle system 
contracts before the apical impulse mass, a physiological fact which 
seems to bear out the latter view and is in agreement with the anatom- 
ical findings of Tawara, that the earliest and most extensive distribution 
of the fibers of the bundle of His is to the papillary muscles. 

We may be reasonably sure that the wave R continues to rise while 
the contraction wave of the ventricle is spreading from base to apex, 
and the simimit of R marks the instant at which this contraction has 
reached the apex of the heart; the time during which this wave R is 
rising is then a measure of the time occupied by the ventricular systole 
in spreading from base to apex, and may well be a matter of value in 
the study of diseases of the heart muscle, for, knowing the distance, it 
is possible to calculate the rate of travel, as has been done by Gotch in 
the exposed heart of the tortoise. During the interval between R and 
T the string remains at zero. This does not indicate a cessation of 
muscular activity, but only that all parts of the muscle are equally 
active and therefore the potential of base and apex remain the same. 



224 



DISEASES OF THE CIRCULATORY SYSTEM 



It is probable that this time period also will be of value in the study 
of the diseased heart. 

R is frequently followed immediately by a negative wave S, the 
significance of which is still in doubt. 

T, the final wave of the ventricular phase of the electrocardiogram, 
is usually directed upward, and therefore indicates relative negativity 
of the base to the apex, that is, a preponderance of basal over apical 
activity at this instant, which is the very end of a ventricular systole. 
From the presence or absence of these several waves, their height, their 
time relations, much valuable information with relation to cardiac irreg- 
ularities has been obtained. For the sake of comparison. Fig. 41, 
giving the curve obtained in a case of auricular fibrillation, is repro- 
duced. The apparatus is too costly and too difficult of maintenance 
to come into general use, but in medical centers it will doubtless be 
found of great value. 

The possibilities of this subject are indicated in the classification of 
cardiac arrhythmias adapted from Erlanger. 

I. Arrhythmia resulting from decreased conductivity in the 
auriculo-ventricular junction — heart-block. A. Partial. — (1) Occa- 
sional ventricular silence. (2) Regularly recurring ventricular silence, 
one ventricular beat to every 7, 6, 5, 4, auricular systoles failing, or a 
2:1, 3:1 or 4 : 1 rhythm prevailing. B. Complete heart-block. — Auricu- 
lar and ventricular rhythm perfect, but independent. C. Paroxysmal 
bradycardia (Stokes- Adams disease) affecting only the ventricular rate. 

II. Arrhythmia from increased irritability. -A. Ventricular extra- 
systoles, independent systole of the ventricle, one or more following a 
normal systole. B. Auricular extrasystoles (including fibrillation of the 
auricles) . 

III. Arrhythmia resulting from the influence of extrinsic nerves 
upon the heart rate. A. Vagus effects. B. Accelerator effects. 

IV. Arrhythmia resulting from disturbed diastolic filling of the 
heart. A. From violent respiratory movements; may give paradoxical 
pulse. B. From adherent pericardium or mediastinal tumor; may give 
paradoxical pulse. C. Associated respiratory and cardiac rhythm. 

Morbid Anatomy. — While changes in the heart muscle itself, either 
primary or secondary to changes in the endocardium, the pericardium 
or other parts, naturally assume the foremost position in this relation, 
and most especially changes in the bundle of His (tumor, sclerosis, 
degenerations, etc.), it is evident that disturbances in the nervous sys- 
tem, the medulla, the vagus and accelerator nerves, induced either by 
local lesions or by changes in remote parts, such as the cerebrum (fear, 
fright, etc.), the digestive organs, the sexual organs (uterus and ovaries 
especially), may profoundly affect the rate and rhythm of the heart 
action. 

Prognosis and treatment must be based upon our views of the 
causation of the arrhythmia. Extrasystoles of either auricle or ven- 
tricle are relatively harmless. 



DISEASES OF THE HEART 



225 



LeadM 



i-'ii iiiiiiiiBi* iirMir^iiiiiiiiiiii''tinwiiiiiii''nimii I'^iimfniiiiiifr'T •inn^'-rni iii*- " tt^i r^n r*"f 



Second 1 



Fig. 41. — Auricular fibrillation in fornplele irregularity. (Am. Jour. Med. Sci., vol. 140, page 662.) 



226 DISEASES OF THE CIRCULATOEY SYSTEM 



Heart-block, either partial or complete, is always serious. Remark- 
able instances of such conditions arising from gummatous infiltration 
and resulting in cure under adequate treatment are on record. 

Fibrillation of the auricles is regularly an end result in failing com- 
pensation and is accordingly of grave significance. Cases are, how- 
ever, known in which this condition has persisted for years. In some 
instances digitalis is very effective, in others it fails. 

ANGINA PECTORIS 

This term is employed by medical writers in two senses: (a) Ety- 
mologically as meaning and including pain of any description referred 
to the heart, (b) Clinically as restricted to a definite disease whose 
chief feature is heart pain. The latter meaning is here employed. 

Etiology. — Heredity is of importance and men over 45 or 50 are 
more frequently affected. 

The causes of arteriosclerosis, especially gout and syphilis, are com- 
monly operative. The disease is rarely seen before thirty-five and is 
common only after fifty. Angina pectoris is often associated with 
aortic valvular lesions. 

Apart from these underlying conditions of the disease the causes op 
THE ATTACKS OF PAIN must be Considered. These may be induced by 
mental excitement or strain, by exposure to cold and wet, by fatigue, 
by attacks of dyspepsia, especially if accompanied by distention, or 
constipation. The use of tobacco, coffee, tea or alcohol is harmful. 

Morbid Anatomy. — A variety of lesions of the heart and arteries 
have been found, including the following: — 1. Changes in the first part 
of the aorta, (a) Direct injury, (b) acute aortitis, (c) atheroma, (d) 
aneurism. 2. Changes in the coronary vessels, (a) Acute or chronic 
arteritis, (b) embolism or thrombosis. 3. Lesions of the aortic valves, 
(a) Stenosis, (b) regurgitation. 4. Myocarditis — fatty or fibroid. 5. 
Degenerative changes in the cardiac ganglia. 6. In rare cases no dis- 
coverable cause. 

Of these changes the most common and most important are the 
arteriosclerosis of the coronary vessels with secondary changes, such as 
thrombosis or embolism and resulting myocardial degenerations. The 
close anatomical relation of the aortic valves to the coronary arteries 
frequently leads to association of their lesions. These lesions explain 
the fatality attending the disease; they do not explain the attacks of 
pain, for they are frequently found in patients who have had no unusual 
pain. 

The paroxysms of pain are variously explained as due (1) to cramp 
of part of the heart muscle, (2) over distention of the ventricles, or (3) 
neuralgia of the cardiac nerves. It is not possible at present to satis- 
factorily decide the problem. 

Symptoms.— Paroxysms of pain referred to the heart are the char- 
acteristic features. The paroxysms come suddenly, often without warn- 



DISEASES OF THE HEART 



227 



ing, sometimes definitely after one of the exciting causes. The pain is 
precordial, sharp or dull, gripping in character, often agonizing, and 
radiates into the neck and left arm, possibly over the whole chest. A 
sense of impending death accompanies it. The duration may be minutes 
or hours. Syncope may occur or death come in any attack. 

Physical Signs. — The patient leans against some support, or sits 
down. The face becomes pale or ashen and expresses intense pain, but 
the patient is quiet or groans, without excitement. The pulse may show 
no change, or may be slow, intermittent and weak, the tension may be 
high or low. Cyanosis or other evidences of circulatory failure are rare. 

The Heart may be enlarged with an apical systolic murmur (dila- 
tation) or may present evidences of any of the lesions of the aortic 
valves and coronary arteries mentioned above. 

After lasting minutes, rarely hours, the pain gradually passes off 
and the patient is left feeling weak and exhausted. The intervals 
between attacks are very indefinite. They may be hours or years. 

]\IiLDER Attacks. — The possibility of milder attacks must be ad- 
mitted, the pain being moderate and very transitory. Occurring in 
patients who are susceptible to severe seizures or who have definite 
evidences of disease of the coronary arteries or myocardium, these may 
be classified as angina pectoris; otherwise as pseudo-angina. 

Diagnosis. — In typical form attacks of angina pectoris can hardly 
be mistaken. The difficulty lies in the milder cases, which may be and 
by some are made to include all varieties of cardiac pain. The two im- 
portant questions are: (1) Have the attacks the character of true 
angina? (2) Are they associated with definite evidences of disease of 
the heart or coronary arteries? In either case they Avould best be re- 
garded and treated as true angina. If both questions can be answered 
in the negative the diagnosis of pseudo-angina may be justified. The 
latter occurs in typical form in women, especially in young women, is 
often related to disturbance of the menstrual function, is accompanied 
by much excitement, often hysterical outcries, there is no evidence of 
arteriosclerosis or disease of the heart, the pulse is rapid and full, the 
face flushed. There are other evidences of hysteria or neurasthenia. 

TOXIC ANGINA 

Attacks of severe pain in the heart region are not uncommon from 
the excessive use of alcohol, tea, coffee, or tobacco. These are met with 
especially in young persons and are associated with palpitation. The 
pain is of shooting character, may be severe, may be accompanied by 
cold sweats and marked prostration. The attacks last several hours and 
may be repeated if the indulgence continues. The age of the patients, 
the history of overindulgence in one of the toxic substances, the absence 
of any signs of disease of the heart or arteries, and the results of absti- 
nence are convincing. 

Prognosis must always be very guarded in true angina. Disease of 
the arteries and myocardium can be safely excluded only after prolonged 



228 DISEASES OP THE CIRCULATORY SYSTEM 



and careful observation. Attacks may occur without warning and any one 
of them be fatal. On the other hand, after one attack the patient may 
escape others and die of old age. Prognosis must be gravest in cases 
in which evidences of disease of the coronary arteries, the aortic valves, 
or myocardium are pronounced. 

Treatment. — The Attacks. — Amyl nitrite, carried in pearls con- 
taining from 3 to 5 minims, one of which is broken in the handkerchief 
and the fumes inhaled, is the most prompt and effective remedy. Nitro- 
glycerine, gr. 1/100 every hour or 2 hours, or erythrol tetranitrate, gr. 
3^ t.i.d., may be used if less rapid effect is desirable. 

Morphine gr. 14 with atropine gr. 1/150 may be given for the pain 
if there is no hypertension or the dilators do not relieve. 

After the attacks rest in bed for several days must be required. 

To Prevent Attacks. — A quiet, even life, free from worry or anxiety, 
in a mild and equable climate, is indicated. (Florida or Southern 
California in winter, the north Atlantic coast in summer are usually 
chosen.) The use of alcohol, tea, coffee, or tobacco is to be forbidden 
or carefully limited. Underlying syphilis or gout must be treated. The 
diet must be simple, and suited to the patient's digestive capacity. The 
daily action of the bowels should be secured. 

The influence of mental excitement, worry, fatigue or exposure must 
be avoided. Simple tonics are given as indicated. In arteriosclerotic 
cases iodide of potassium, 3 to 5 grains thrice daily, should be given for 
long periods. 

CONGENITAL DEFECTS OF THE HEART 

Rare even in post-mortem work in infants, congenital defects of 
the heart are very uncommon in clinical work, because for the most part 
incompatible with life beyond a few days or weeks. The following 
lesions are, however, occasionally met with, in children or young adults: 

(1) Patent foramen ovale. (2) Pulmonary stenosis (q. v.). (3) 
Patent ductus Botalli. Of these pulmonary stenosis is the most com- 
mon and most important. The importance of patent foramen ovale, 
usually given as the commonest type of congenital lesion, is doubtful. 
It is most common, for it occurs regularly with the other lesions men- 
tioned above, and it is met independently. So long, however, as there 
is no impediment to the onward passage of the blood and the two 
auricles contract synchronously, it is difficult to see how this defect can 
in any degree affect the circulation or give rise to physical signs. On 
the other hand, in conditions such as pulmonary stenosis it may favor 
the equalization of pressure in the auricles. 

The symptoms of congenital lesions of the heart are given under 
Pulmonary Stenosis. The physical signs include cyanosis, clubbing 
of the fingers, enlargement of the heart and murmurs of bizarre 
character. 

The DIFFERENTIAL DLVGNOSis of pulmonary stenosis has already been 



DISEASES OF THE ARTERIES 



229 



given. -If the signs warrant that diagnosis, it may be advanced; other- 
wise we can only speculate as to the anatomical condition. 

Prognosis. — Few ''blue babies" survive the early months of 
infancy ; rarely do they reach puberty. Yet they may with care do so. 

Treatment. — The lines of treatment for acquired lesions must be 
followed. Protection from acute infectious diseases, avoidance of car- 
diac strain and care of the general health are most important. With 
signs of increasing dilficulty, rest, the administration of digitalis and 
the other measures outlined on page 204 may be employed. 

DISEASES OF THE ARTERIES 

ACUTE AORTITIS 

Acute inflammatory lesions of the arch of the aorta are occasionally 
seen as part of an acute endocarditis, particularly in lesions of the 
aortic valves. Very rarely indeed is the condition met with independ- 
ently. In such cases it will almost surely be mistaken for aortic stenosis, 
the two conditions being often associated and the physical signs and 
symptoms being practically the same. 

ARTERIOSCLEROSIS— CHRONIC ARTERITIS 

Definition. — A general thickening of the walls of the arteries with 
degenerative changes, especially in the intima. Various terms are applied 
to the process. In the larger vessels it is commonly called atheroma; 
when the degenerative changes in the intima are unusually marked, 
endarteritis deformans or obliterans. 

Etiology. — 1. Age. — Degeneration of the arteries belongs to ad- 
vancing years and in most persons over forty is present to some degree. 
These changes are, however, hastened and. intensified by many influences. 

2. Heredity. — In certain families arterial degeneration occurs early 
and is unusually marked. 

3. Sex. — Men, more than women, are subject to the influences pro- 
ducing arteriosclerosis. 

4. Chronic infections or intoxications, including syphilis, gout, 
rheumatism, diabetes. Of these syphilis is by all means most important. 
In this case a definite infection is present. 

In the other instances chemical poisons, such as lead or uric acid, 
are concerned. Alcohol and tobacco are regularly enumerated under 
this head, but there is no agreement as to their influence. 

5. Conditions causing persistent high arterial tension, (a) Con- 
tinued hard muscular work. The laboring man often shows early arterio- 
sclerosis, (b) Overeating and drinking. The constant overloading of 
the circulation with excessive amounts of food material, even in tee- 
totalers, results in harm from high pressure, (c) The stress and strain 
of modern life seem to bring about high tension independently of other 



230 



DISEASES OF THE CIRCULATORY SYSTEM 



influences, (d) Chronic Bright 's disease. High tension is often asso- 
ciated with chronic nephritis, especially the interstitial type. Either 
may be the primary affection. 

Morbid Anatomy. — The lesions of arteriosclerosis are usually wide- 
spread, affecting more or less evenly all the arteries of the body, and 
showing especially in the aorta. In rare instances the lesions are un- 
evenly distributed and we find the arteries of particular territories 
showing marked changes while others are but slightly involved. In like 
manner the individual vessel usually shows changes in all its coats, but 
in most cases the changes in the intima and median coats are most im- 
pressive. Several types of arteriosclerosis may be distinguished. 

1. Circumscribed or nodular form, best seen in the aorta and larger 
arteries. In the early stages small yellowish placques or nodules appear 
in the intima, slightly raised, smooth. Later the placques become larger, 
more raised, then ulcerated, the intima being destroyed, and finally 
infiltrated with lime, forming more or less extensive areas in the wall 
of the vessel with an excavated, rough, irregular surface, of almost stony 
hardness. Such areas may quite surround the lumen of the vessel. The 
surface may show small thrombi. The vessel wall is distorted in form, 
thickened by connective-tissue formation or thinned by the necrosis and 
ulceration and dilatation, and may be the seat of aneurismal sacs. 

Microscopically the vessels show a round-celled infiltration, or 
necrosis in the media, especially about the vasa vasorum, increase in 
connective tissue, fatty degeneration of the intima and of the muscular 
coats. The elastic layer also is thinned and degenerated. The primary 
changes are those of the median coat. 

The result of the circumscribed arteriosclerosis is to produce in the 
walls of the aorta and greater arteries localized areas of weakness and 
distortion, which may become dilatations or even ruptures, which may 
give rise to thrombi and infarctions or which may seriously disturb the 
circulation directly or indirectly by involving the moutlis of branch 
vessels. 

2. Generalized Arteriosclerosis. — In this process the arteries through- 
out the body are more or less evenly involved. The gross changes are 
greater thickening of the walls of the vessel (so that arteries like the 
radial become palpable) and greater tortuosity. On opening the thick- 
ened vessels they may appear normal, or the lumen may be distorted, or 
minute dilatations may appear and the intima may here and there show 
placques of degeneration such as belong to the circumscribed form. 

Microscopically the most striking change is the increase in the con- 
nective tissue and muscle fibers of the median coat, gi^nng the greater 
thickness to the vessel wall. These changes are best seen in the periph- 
eral vessels. The thickened wall may be infiltrated with small round 
cells and its tissues may show various degenerations. The intima may 
present areas of hyaline or fatty degeneration. The elastic and muscular 
coats are thinned and degenerate. 

These changes in the smaller arteries are regularly accompanied in 



DISEASES OF THE ARTERIES 



231 



some parts, especially the aorta, by the changes of the circuniscribed 
form. 

The results of generalized arteriosclerosis are thickening of the 
peripheral vessels with some loss of elasticity. These changes increase 
the resistance to the circulating blood, raise the blood-pressure and lead 
to hypertrophy of the left ventricle with ultimate dilatation. 

The kidneys are regularly involved in the process. They are of 
normal size or small, the capsule is adherent, the surface somewhat 
rough, the cortex firm, and microscopically there is increase of con- 
nective tissue and changes more or less closely approximating those of 
chronic interstitial nephritis. 

3. Senile Arteriosclerosis. — The walls of the larger arteries are 
stretched, thin, stiff and tortuous. There are degenerations of both 
intima and media closely resembling those seen in the diffuse process. 
The viscera are atrophic, the heart is not enlarged or hypertrophied, and 
is often smaller than normal, with thin, deep-browTi muscle, the so-called 
brown atrophy. 

Symptoms. — The relation of high blood-pressure and arteriosclerosis 
has been much discussed. Which is primary? Are they produced by 
the same cause and at the same time ? At any rate they are closely asso- 
ciated and with thickening of the radial and other palpable arteries 
there is hypertrophy of the left ventricle (see p. 208) and accentuation 
of the second aortic sound. By this compensatory hypertrophy the 
heart is able to drive the blood through the narrowed and stiffened 
arteries and maintain for a time normal circulation. In the end the 
heart fails or the advance of the disease in some one territory develops 
symptoms relative to that part. The symptoms of arteriosclerosis may 
therefore be grouped as follows : 

1. Cardiac. — Dilatation of the heart with all the symptoms of cardiac 
failure may come at any time. Dyspnea, cyanosis, edema, etc., occur as 
in any such failure. The heart is dilated and there are murmurs of 
insufficiency over the mitral and possibly the aortic valves. These cases 
are therefore easily mistaken for endocarditis with dilatation, but in 
many cases despite the signs of failure the blood-pressure is inordi- 
nately high — 200 mm. or more. 

Disease of the coronary arteries, fibroid myocarditis, or angina 
pectoris may complicate the condition. 

2. Cerebral. — Headache, dizziness, insomnia, or sudden attacks of 
vertigo are characteristic. The cerebral disturbance may be severe. 
The attacks of vertigo, temporary unconsciousness, or paralysis (hemi- 
plegia, monoplegia or aphasia) are particularly suggestive in elderly 
persons. These attacks may be repeated frequently and may be re- 
peatedly recovered from, but at any time may be followed by cerebral 
hemorrhage and permanent disability. 

3. Renal. — Some of the cases terminate as chronic interstitial 
nephritis and it may be impossible to determine whether the kidney or 
the arterial disease was primary. 



232 DISEASES OF THE CIRCULATORY SYSTEM 



4. Gangrene of the extremities (legs) may occur, especially in cases 
in which chronic nephritis or diabetes is present. 

5. Cramps in the legs or abdomen, intermittent claudication, may 
appear. The cramps usually follow effort and are relieved by rest, but 
the reverse relation may prevail. 

Course. — Once the compensation is disturbed or symptoms relative 
to any one part are developed, the disease is ordinarily slowly progressive 
and fatal in the course of a few years at most. The prognosis in any 
case depends largely upon the condition of the heart and kidneys and 
the patient's ability to lead a quiet, easy life. 

Treatment. — All possible harmful influences such as alcohol, tea, 
coffee or tobacco should be regulated or cut off. Hard work of body 
or mind should be forbidden. 

A moderate diet with abundance of water, and moderate daily ex- 
ercise (walking, golf, driving, etc.) should be ordered. Red meats 
should be used sparingly and the use of fruits and vegetables enjoined. 
The bowels should be kept freely open and the skin active. Iodide of 
potassium in small doses should be given for long periods. Unless the 
heart is failing the high tension of the pulse is best regulated by these 
measures. If it must be more rapidly reduced, nitroglycerine gr. 1/100 
every two hours, or erythrol tetranitrate in doses of I/4 to i/^ grain thrice 
daily may be tried. Often all these remedies fail. 

Special symptoms relating to brain, heart or kidney must be treated 
as required. 

Patients with arteriosclerosis do well to spend their winters in the 
milder climates of the south or southwest, their summers at the north. 
Often residence for a time at one or another of the various European 
spas is beneficial. 

ANEURISM 

Definition. — A circumscribed dilatation of an artery. A number 
of forms of aneurism are described. The true aneurism only is here 
considered. (1) A true aneurism is one whose sac is formed by one or 
more of the coats of an artery. (2) A false aneurism is in reality a hema- 
toma lying in connection with a vessel but surrounded only by connective 
tissue, not the walls of the artery. (3) A dissecting aneurism is a dilata- 
tion of an artery by blood lying within the sheaths of the vessel itself. 
Such dissecting aneurisms are fo\ind chiefly in the thoracic or abdominal 
aorta. (4) A miliary aneurism is simply a minute dilatation of an 
artery, most often seen in the cerebral vessels. (5) Arterio-venous 
aneurisms are formed by direct communications between an artery and 
vein, such as the aorta and the superior vena cava. If a sac is formed 
between the two vessels it is called a varicose aneurism ; if there is no sac 
and the vein is most dilated, an aneurismal varix. (6) A cirsoid aneur- 
ism is a general dilatation of an artery and its branches. They are most 
often seen in the arteries of the scalp. (7) IMycotic aneurisms are 
sometimes seen in malignant endocarditis from weakening of the wall of 



DISEASES OF THE ARTERIES 



233 



an artery produced by the lodgment of infected emboli. (8) In form 
aneurisms are classified as sacculated, when involving only a circum- 
scribed part of the artery, or as fusiform or cylindrical when the entire 
circumference of the vessel is involved. 

Etiology. — Two factors are ordinarily concerned: (1) Weakening of 
the wall due to arteriosclerosis. Any of the causes of this condition 
may be operative, but syphilis is particularly effective, being present 
in 75 per cent, of all cases. (2) Increased blood-pressure. Any 
rise of pressure may cause dilatation in a weakened vessel. Heavy 
lifting or other severe physical exertion is often responsible for the 
condition. By reason of this etiology aneurisms are therefore seen most 
often in middle life, and in men rather than women. Congenital 
aneurisms are recorded, but are very rare. 

Morbid Anatomy. — In the aorta, with which we have commonly to 
deal, an aneurism forms a tumor, in the case of the fusiform or cylin- 
drical aneurism having the general contour of the vessel more or less 
enlarged, or in the sacculated form projecting from one side of the 
vessel and connected to its lumen by a larger or smaller orifice. Much 
inflammatory thickening may be present about the tumor, but the walls 
of the vessel itself are thinned and at autopsy often ruptured at one 
point. Rupture may have occurred externally through the thoracic 
wall, or internally into the pleura, pericardium or any of the adjacent 
hollow organs, the trachea, esophagus, or even stomach. 

On opening an aneurism the inner surface is commonly roughened 
and covered by clots. Occasionally an aneurism is found in which 
clotting and organization of blood have occurred in successive layers 
till the cavity of the vessel has been more or less completely filled by con- 
nective tissue and the opening into the aorta closed (normal healing) . 

Ifi other cases the original walls of the aneurism are greatly thinned, 
the intima more or less completely destroyed, and the roughened internal 
surface of the sac covered with layers of fibrin. 

About aneurisms of any size there are evidences of pressure, such 
as erosion of sternum and ribs or even the bodies of the vertebra, com- 
pression of one or more lobes of the adjacent lung, displacement and 
erosion of the trachea and larger bronchi or the esophagus. 

The heart is usually hypertrophied and dilated by the influences which 
have caused the aneurism, or it may be displaced. 

The aorta and arteries show more or less arteriosclerosis and the 
kidneys are the seat of chronic nephritis. 

Symptoms. — An aneurism is a pulsating tumor which tends to 
slowly but steadily enlarge. The symptoms produced by it are due 
to pressure and in the thorax therefore depend greatly on the posi- 
tion and size of the aneurism. The anatomical relations of the several 
parts of the aorta must be borne in mind. Aneurisms of considerable 
size may give no signs until rupture occurs or they may be discovered 
only post-mortem. Some give notable physical signs without symp- 
toms, especially those of the ascending part of the arch, others on the 



234 DISEASES OF THE CIRCULATORY SYSTEM 



transverse arch, symptoms without signs, while if placed on the descend- 
ing thoracic aorta they often give neither signs nor symptoms. 

Pain due to pressure is the most constant symptom. The pain is 
either dull or sharp, located over the base of the heart, and often radiates 
into the neck or arms. 

Dyspnea and cough either constant or paroxysmal are usually pres- 
ent, owing to pressure upon the trachea or bronchi. Expectoration, 
usually mucous, but sometimes bloody, accompanies the cough. Other- 
wise the symptoms vary with the location and are best considered 
accordingly. 

I. Aneurism of the ascending portion of the arch — the 
ANEURISM OF PHYSICAL SIGNS (Broadbent). — Pain is caused by pressure 




Fig. 42. — An aneurism of the arch of the aorta. From the collection of Dr. Walter B. James. 



on the sternum or ribs, dyspnea by interference with the right bronchus, 
cardiac distress and palpitation by embarrassment of the heart action — 
through high blood-pressure and secondarv aortic incompetencv. (Fig. 
42.) 

Physical Signs. — (a) Bulging of the thoracic wall at or near the 
level of the second right costal cartilage, (b) Pulsation visible and 
palpable and a thrill in the first, second or third right space, (c) 'Move 
or less extensive dulness in the same position, (d) ^lurmurs over the 
tumor. A systolic murmur long, loud, harsh, due to the aneurism and 
followed by the diastolic murmur of aortic incompetency, Avhich can be 
traced downward beneath the sternum and to its left, (e) The veins of 
the right thorax may be enlarged by pressure on the internal mammary 
or the head and neck may show cyanosis from obstruction of the 



DISEASES OF THE ARTERIES 



235 



superior cava, (f ) The tumor may erode the thoracic wall and present 
itself covered only by the thin and congested integuments. It may rup- 
ture into the pleura, pericardium, or the superior cava, or through the 
skin. 

The condition terminates in one of several ways : — 
1. Rupture into the pericardium may be quickly fatal. If slow, 
there is precordial pain with a rapid pulse, increasing dyspnea and 
cyanosis. At first there are sounds resembling pericardial friction, later 
the area of cardiac dulness increases, the heart sounds become faint, 
the pulse rapid, feeble and irregular, giving the clinical picture of 
pericarditis with effusion. Fever may be present. 2, Rupture into the 
vena cava is consistent with life for several months. A sudden conges- 
tion of the head and face with cyanosis and later edema develops. Over 
the base of the heart is heard a continuous loud ''boiling" murmur 
rising and falling with the systole and diastole of the heart and trans- 
mitted widely. There is great distention of the veins of the head, neck, 
arms, and upper thorax. 3. Rupture into the pleura (right) or lung 
w^ill cause collapse and hemoptysis or signs of effusion in the pleura. 4. 
Rupture externally, death from hemorrhage. 5. Cardiac failure second- 
ary to aortic insufficiency. This is perhaps the most common ending. 

II. Aneurism op the Transverse Arch. — Aneurism of Symptoms. 
— 1. Pain may be slight or severe. 2. Dyspnea is usually marked from 
pressure on the trachea and bronchi. Its paroxysmal character is nota- 
ble. 3. The voice is sometimes hoarse and feeble with a brassy cough, 
due to pressure paralysis of the left recurrent laryngeal nerve as it winds 
round the aorta. 4. Difficulty in swallowing may be caused by pressure 
on the esophagus. 

Physical Signs.— (1) The tumor presents behind or above the 
manubrium, or immediately to the right or left, with corresponding 
impulse and dulness (see Fig. 26). (2) A tracheal tug may be ob- 
tained. If the patient's head be held back so as to greatly stretch the 
trachea, and the lower edge of the cricoid cartilage be grasped by the 
examiner's fingers, with each pulsation a distinct do^^^lward tug may be 
felt as the expansion of the aneurism drags down the trachea. 

(3) The radial pulses may be unequal, the left being smaller, and 
somewhat delayed, rarely it may be obliterated. The explanation 
may be the loss of the pulse wave in a large sac lying between the right 
innominate and the left subclavian arteries, or pressure upon the latter 
vessel or its obliteration by advanced sclerosis. 

(4) Pressure on the left innominate vein mav cause dilatation of 
the veins of the left side of the head, neck and thorax with cyanosis 
(see Fig. 43). 

(5) Pressure on the trachea or bronchi may give rise to signs of 
obstruction to the entrance of air into the lung, especially on the left 
side. The lung may be compressed or hydrothorax follow. 

(6) Pressure on the left sympathetic nerve may cause dilatation of 
the left pupil and flushing or sweating of that side of the face. 



236 DISEASES OF THE CIRCULATORY SYSTEM 



(7) A sharp diastolic shock due to the closure of the aortic valves 
under pressure may be felt if they are competent. 

(8) The tumor may erode the sternum or ribs and present exter- 
nally. 

III. Aneurism of the Descending Part of the Arch. — Deeply 
placed, close to the vertebral column, these aneurisms rarely give definite 
physical signs. Erosion of the bodies of the fourth and adjacent dorsal 
vertebrae causes pain in the back or radiating around the thorax like 
that of caries of the spine. The spine may be deformed as in the latter 
condition. The possibility of aneurism must always be remembered in 
adults presenting signs of caries of the micl-dorsal spine or a pressure 




Fig. 43. — Edema of the face and arms caused by the pressure of an aneurism of the arch of the aorta. 

paralysis of the lower extremities. A systolic murmur may be heard 
in the back and dulness and possibly pulsation observed in the back 
close to the left side of the fourth dorsal spine. 

IV. Aneurism op the Thoracic Aorta. — This differs in no essential 
particular from the last, except in the lower situation of the pain and 
the phj^sical signs if obtained. 

V. Aneurisms op the Abdominal Aorta. — Any part of the great 
trunk or of its branches may be affected, yet aneurisms of this part are 
rare as compared to those of the thoracic aorta. The commonest site 
is just below the diaphragm, where the aneurism may become large before 
being discovered. 



DISEASES OF THE ARTERIES 



237 



The SYMPTOMS are those of tumor, pressure upon surrounding vis- 
cera or the spine. 

The Physical Signs. — Pulsation may be seen in the epigastrium. 
The tumor may be visible as well as palpable. The expansile pulsation 
is characteristic. A systolic murmur may be heard over the tumor, and 
if superficial, dulness may be obtained. 

Diagnosis of Abdominal Aneurism. — In neurotic persons the aorta 
often displays an abnormal pulsation, and aneurism is suggested. Care 
must be taken to identify a tiunor as distinguished from the normal out- 
lines of the aorta. 




Fig. 44. — Aneurism of the arch of the aorta vdewed from behind. The heavy shadow bulging to the 
right of the median line is the dilated aorta. Compare w'th the normal heart seen in Fig. 7. 

Tumors overlying the aorta may pulsate, but on grasping them the 
expansile pulsation of an aneurism is lacking. 

Ruptured abdominal aneurisms, the blood being retroperitoneal, have 
repeatedly been mistaken for rapidly growing, malignant tumors. 

Diagnosis of Thoracic Aneurism. — Persistent pain in the chest of 
an adult should always suggest aneurism. Careful examination may dis- 
close signs otherwise easily overlooked. A history of syphilis is sug- 
gestive. 

Cardiac lesions, especially aortic regurgitation, give similar symp- 



238 DISEASES OF THE CIKCULATORY SYSTEM 



tonis and signs. Extreme aortic stenosis may do the same. ^Marked 
enlargement of the heart is in favor of valvular lesions, but the dis- 
placement produced by aneurism may give the impression of great 
enlargement. 

^Mediastinal tumors overlying the aorta may pulsate. The thrill^ 
murmurs and diastolic shock are absent. 

Tuberculosis is frequently simulated by aneurism because compres- 
sion of a bronchus may give rise to dulness and changes of voice and 
breathing, and vocal fremitus, while the congestion causes hemoptysis. 
Bacilli are absent. 

Obstruction of the esophagus may suggest stricture and the possi- 
bility of aneurism must always be remembered in these cases. 

Caries of the spine in an adult may be due to aneurism. 

The most effective means of demonstrating or excluding aneurism 
of the aorta is the radiograph. Xo other means approaches it in accu- 
racy. In hospitals where the X-rays are regularly employed, aneur- 
isms are now rarely missed. (See Fig. 44.) 

Prognosis. — The outlook is always grave, the duration of life after 
the onset of symptoms is usually not more than a few years and some 
cases are rapidly fatal. On the other hand, life may be prolonged for 
ten or fifteen years and the possibility of spontaneous healing cannot 
be denied. 

Treatment. — Eest is the first requirement, with a light diet and 
restriction of fluids to a minimum. In well-nourished, vigorous men 
Tufnell's starvation plan may be tried. This allows but ten ounces of 
solid food and eight ounces of fluid per day. By these means the fre- 
quency 'of the heart beat and the blood-pressure are reduced while the 
coagulating povrer of the blood is increased. Calcium lactate may be 
given for its influence in the latter direction. Iodide of potassium, ten 
grains thrice daily, is commonly prescribed. The bowels must be regu- 
larly moved without straining. To be effective such treatment must 
be carried out for weeks or months. In most cases some amelioration 
is secured. 

]\Iorphine may be given for the relief of pain or dyspnea. If hydro- 
thorax arises, frequent tapping may be required. Venesection may be 
emploA^ed for cyanosis. 

Surgical Methods. — Coagulation of blood in the sac has been pro- 
moted in a few cases by the introduction of silver wire through a fine 
needle passed into the aneurism. ]\Iany feet of wire have thus been 
reeled into the sac, and coagulation still further favored by the passage 
of galvanic currents through the wire. These methods have been more 
successful in abdominal than in thoracic aneurisms and their very 
limited success has not led to their general adoption. 

Injections of 2 per cent, gelatin in normal salt solution, 3 ounces 
given every other day, with the purpose of furthering clotting have 
been tried. Tetanus has resulted in some instances, but can be avoided 
by thorough sterilization. They have but little influence. 



DISEASES OF THE VEINS 



239 



DISEASES OF THE VEINS 

ACUTE PHLEBITIS 

Etiology. — Acute inflammation of the veins may occur as the result 
of various causes. (1) Trauma, especially in the case of the superficial 
veins. (2) Extension of inflammation from adjacent foci. Thus in 
suppurative otitis media and mastoiditis, the jugular vein may be in- 
volved ; widespread inflammation of the uterine veins accompanies endo- 
metritis ; about the diseased appendix or suppurative processes in the 
bones the veins may be extensively diseased. (3) In many of the acute 
infectious diseases, especially typhoid fever, septicemia, pneumonia, in- 
fluenza, syphilis, and tuberculosis, phlebitis develops. In some of these 
cases the inflammation of the veins is explained by extension from some 
local focus of infection, in others the phlebitis occurs at a distance from 
any such foci and must be explained by the presence of organisms or 
toxins in the blood, and possibly by previous local injury or sclerosis 
of the vessel. (4) In severe anemia or cachexia phlebitis is not 
uncommon. 

(5) Finally a certain group of cases is known in which phlebitis 
occurs without apparent cause (idiopathic) and in which the disturb- 
ance is attributed to gout or rheumatism. In many of these cases the 
existence of either gout or rheumatism is as doubtful as their rela- 
tionship to the phlebitis when they are definitely established. 

Morbid Anatomy. — Any or all of the coats of the vein may be in- 
volved, so that in some instances we speak of an endophlebitis, in others 
of a periphlebitis. Inflammation of a vein is regularly accompanied by 
thrombosis of varying extent. If the process be limited to a peri- 
phlebitis, thrombosis may not occur. 

All grades of acute inflammation may be observed in the veins, 
from slight thickening due to infiltration of the walls to suppuration 
and complete destruction of parts of the vein. The microscopic picture 
varies accordingly. The thrombi are pale red or gray, adherent to the 
walls of the vein, and composed largely of fibrin or granular material 
mingled with blood cells. These thrombi may break down into abscesses, 
if infected, or they may become fibrous and permanently occlude the 
vein or be absorbed with restoration of the circulation. 

Effects of Phlebitis. — If the vein remain patent, phlebitis declares 
itself only by the signs of local inflammation, pain, tenderness, etc. 

In most cases the vein is obstructed, and the blood dammed back in 
the territory affected, with resulting congestion and edema. The per- 
manency of these changes depends upon the fate of the thrombus and 
the efficiency of the compensatory circulation. (See Fig. 45.) In the 
viscera thrombosis; of a vein has much the same effect as that of an 
artery, producing, as a rule, wedge-shaped areas of deep congestion 
which may suppurate, or undergo gradual transformation like an infarc- 
tion (see p. 16). 



240 DISEASES OF THE CIRCULATORY SYSTEM 



In the extremities the obstruction to circulation may be temporary 
or permanent. 

Symptoms. — General. — There are usually none, unless the phlebitis 
be of infective origin, when there may be a septic fever and the accom- 
panying rapid pulse, prostration, sweating and anemia. If the phlebitis 
be extensive a moderate fever may be present, even in the non-infective 
cases. 

Local. — Pain, tenderness, some thickening of the vein, and possibly 
redness are present. The vein can usually be felt as a thickened and 
tender cord, especially in the extremities. Edemxa commonly develops 
in the territory drained. Thus in jugular thrombosis, edema may be 




Fig. 45. — Dilatation of the superficial veins of chest and abdomen secondary to occlusion of the superior 
vena cava caused by pulmonary and pleural tuberculosis. 

found over the mastoid and adjacent parts of the skull, and tenderness 
and possibly thickening of the vessel in the neck. In the lower extremi- 
ties the thickened femoral or saphenous vein is easily felt, the overlying 
tissues may be reddened and swollen, and edema of the foot and leg 
below the lesion develops. 

The active symptoms subside in two or three weeks, but especially 
in the lower extremity obstructive symptoms, swelling and edema, with 
some difficulty in walking, persist for months or years, depending upon 
the extent of the thrombosis, its permanency, and the development of 
compensatory circulation. 

Embolism. — Any thrombosis of a vein may be the source of an 
embolus, but fragments are particularly likely to separate from infected 



DISEASES OF THE VEINS 



241 



and softening thrombi and thus be carried to the liver, if the primary 
focus lie in the territory of the portal vein, or to the lungs, if the sys- 
temic veins are concerned. Apparently minute emboli may pass through 
the capillaries of the lungs, reach the left side of the heart and be car- 
ried to any part of the periphery, the brain, spleen, kidneys being espe- 
cially often their final lodgments. The results of such emboli depend 
partly upon the site in which they lodge, and whether they are infected 
or not. Sterile emboli produce the phenomena of infarction (see p. 16). 
Infected emboli may excite a suppurative inflammation or abscess where 
they lodge, but do not always do so. Especially is this true of the 
emboli derived from the heart in cases of septicemic endocarditis. The 
relationship of septic thrombophlebitis to pyemia is pointed out on 
page 375. 

Special Varieties of Acute Phlebitis. — Of the Jugular Vein. — In- 
flammation of the lateral sinus and the jugular vein follows otitis 
media or mastoiditis, and is therefore regularly suppurative in char- 
acter. It constitutes one of the most dangerous complications of these 
conditions, as from its nature it may terminate either in suppurative 
meningitis or pyemia. 

The symptoms are not easily differentiated from those of the pri- 
mary conditions. Fever, frequently interrupted by chills, headache, 
vomiting and marked prostration are commonly observed. Locally there 
may be edema and tenderness over the mastoid, sometimes tenderness 
of the jugular vein in the neck, but often these local signs are wanting 
and the diagnosis is made only on exposure of the lateral sinus in the 
course of an operation on the mastoid. The presence of an old suppura- 
tive otitis media with the onset of the above symptoms, and a leukocy- 
tosis, without other discoverable cause are the important points in diag- 
nosis. Blood cultures are usually positive. The treatment is purely 
surgical, the ligation of the jugular vein and removal of the infected 
clot found in the sinus and vein. 

Of the Appendicular Veins. — The veins of the appendix are for 
the most part tributaries of the portal system, but through the external 
or retro-colic veins communication is established with the inferior vena 
cava. Inflammation of these veins of varying severity occurs in appen- 
dicitis. Thrombosis follows and emboli may be carried to the liver or 
lungs. If the emboli be infected abscesses may result. The rapidly 
fatal embolism of the pulmonary artery which follows, in some instances, 
operations upon the appendix, is believed to have its origin in this 
thrombophlebitis of the veins of the appendix. 

Of the Femoral Veins. — This is the most common type of thrombo- 
phlebitis. It may occur under any of the conditions given as producing 
phlebitis, but is especially common as a complication of the puerperium, 
of typhoid fever, and operations upon the abdominal organs. It is much 
more frequent on the left than on the right side. 

The inflamed veins can usually be felt as a tender cord either imme- 
16 



242 DISEASES OF THE CIRCULATORY SYSTEM 



diately below Poupart's ligament or in the middle third of the thigh. 
Edema of the foot and leg is usually present. 

Treatment. — The indications are to allay pain, limit the thrombosis, 
favor the circulation and provide, so far as possible, against the dangers 
of embolism. 

The coagulability of the blood should be tested, and, if increased, 
efforts should be made to lower it by the free administration of water 
and lemon juice (citric acid). The juice of half a dozen lemons may 
be given daily. For the relief of pain an ice-cap should be applied to 
accessible veins. In the early stages morphine may be required. The 
circulation is to be favored by elevating the affected part, leg or arm, 
to aid the venous return. Absolute quiet of the affected part should be 
enjoined and, if necessary, enforced by the use of a splint. Ordinarily 
the leg or arm is made comfortable on pillows and the patient instructed 
to avoid all active motion. 

The duration of this period of quiet varies in different cases. It 
must at least be maintained till all local pain and tenderness have dis- 
appeared and the danger of embolism is passed, a period of three weeks 
in most cases of femoral phlebitis and sometimes much longer. 

Active movement of the affected part should be begun cautiously and 
gradually increased. If edema persists, massage may be employed, but 
this should likewise be used with caution and any manipulation of the 
affected vein or veins avoided. The wearing of an elastic stocking may 
eventually be necessary. 

THROMBOSIS 

Definition. — Thrombosis is the formation of a solid mass or plug in 
the living heart or vessels from the constituents of the blood (Welsh). 

Etiology. — The most familiar example of thrombosis is the clot 
which plugs a ligated artery or vein. The injury done the intima of 
the vessel and the stopping of the blood stream are here the most im- 
portant factors. Clinically we see many examples of thrombosis occa- 
sioned by disease of the walls of blood vessels, arteritis or phlebitis 
resulting in the formation of atheromatous areas in the intima (see 
Phlebitis, p. 239). But thrombosis undoubtedly occurs in vessels whose 
walls are normal, and the cause of the condition must then be sought 
in changes in the biochemical composition of the blood leading to its 
readier coagulation and to slowing of the blood stream. Under ordinary 
conditions the factors necessary to coagulation of the blood, thrombogen 
(fibrinogen) and thrombokinase (fibrin ferment), are not present as 
such in the blood, but are promptly developed Avhen the blood escapes 
from the vessel into the tissues, for the prothrombogen of the blood 
then quickly becomes thrombogen and the thrombokinase is found in 
the vessel wall, in muscle and glandular tissues and is probably de- 
veloped from the decomposition of red blood cells. What the conditions 
which introduce these processes Avithin the vessels are, we do not know. 

Impairment or stoppage of the circulation favors clotting within the 



DISEASES OP THE VEINS 



243 



vessels, and thrombosis is therefore often seen in circulatory failure, 
especially in those forms due to disease of the heart. 

Bacteria and their toxins favor thrombosis by injuring the walls of 
the vessels, rather than directly by their owtl presence, and the throm- 
bosis thus caused is secondary to the arteritis or phlebitis. 

The morbid anatomy of thrombosis is that of phlebitis except for 
the absence of changes in the vessel wall. Arterial thrombosis has the 
same results as an embolus. 

The symptoms of thrombosis are those of phlebitis (see p. 240), except 
that the local signs are less marked. They may indeed be absent and 
the only evidence of the thrombosis consist of swelling and edema of 
the affected parts. The most familiar type of the thrombosis is seen in 
the brachial or axillary veins in the broken compensation of cardiac 
disease. 

Special Types. — Thrombosis of the superior vena cava may occur, 
usually from pressure upon the vessels by aneurism, tumor or cica- 
tricial processes, such as chronic pleural tuberculosis. If the process 
is rapid, death is immediate. If slowly developed, the obstruction is 
compatible Avith life for years. In these cases remarkable dilatation of 
the superficial veins of the thorax occurs (see Fig. 45). 

Thrombosis of the inferior vena cava may occur, producing edema 
of the legs and back without ascites. 

Thrombosis of the portal vein may also result from compression or 
from disease of the wall of the vein. This condition has been observed 
in a number of cases of Banti's disease, splenomegaly with recurrent 
ascites. The condition is most often mistaken for atrophic cirrhosis of 
the liver. 

Thrombosis of pulmonary vessels is not to be distinguished from 
pulmonary infarction. 

Cardiac thrombi are frequently seen, especially in septicemic endo- 
carditis. Large thrombi are occasionally observed in the heart, espe- 
cially in the auricular appendages in cases of simple chronic endo- 
carditis. The formation of large thrombi is occasionally the immediate 
cause of death, but the symptoms and physical signs are too confusing 
to permit of diagnosis. 

The treatment of thrombosis, when practicable, is that of phlebitis. 

HEMORRHOIDS 
(Piles) 

Definition. — A localized or diffuse dilatation of the hemorrhoidal 
veins, especially of the anal plexus. If within the external sphincter, 
the hemorrhoids are spoken of as internal, as external if they involve 
the veins without the external sphincter. Often the two conditions are 
associated. 

Etiology. — (1) The chief factors are mechanical, increasing the 
pressure within the veins, (a) The upright position naturally increases 



244 



DISEASES OF THE CIRCULATORY SYSTEM 



the influence of gravity, (b) Constipation and straining at stool, (c) 
Stricture or other tumor of the rectum, (cl) Tumors of the uterus or 
other abdominal organ pressing upon the rectum, (e) Pregnancy, (f ) 
Portal obstruction of any kind, especially atrophic cirrhosis of the liver. 
(2) Conditions producing relaxation of the tissues concerned, (a) Old 
age. Hemorrhoids are rare in childhood and increase steadily in fre- 
quency with the years, (b) Debility from any cause. 

Symptoms. — Piles of considerable size may give no symptoms and 
are often discovered in the course of routine physical examination. Dis- 
turbances of sensation, itching, burning, or pain, and hemorrhage con- 
stitute the chief symptoms of this condition. Itching or burning about 
the anus may produce great distress and the resultant scratching often 
causes eczema, erosions, or fissures of the anus. Pain is usually mod- 
erate, and is referred to the anus or adjacent parts, unless intensified by 
complications. These are frequent. Internal hemorrhoids are often 
protruded during the act of defecation and are then gripped and 
strangulated by the sphincter. Gentle pressure at first reduces the mass 
and relieves the condition, but at any time may prove ineffective. The 
patient suffers intense pain, radiating into the extremities, and the 
condition steadily grows worse, the hemorrhoidal mass becomes inflamed, 
swollen, possibly ulcerates. Sepsis or pyemia may result. External 
hemorrhoids frequently become the seat of thrombophlebitis, which 
causes swelling with great tenderness, so that the patient cannot sit 
down, and severe pain. 

Constipation, one of the chief factors in the production of piles, may 
also result from their presence, the pain excited by defecation tending 
to inhibit the action. 

Hemorrhage is a common occurrence from either internal or external 
hemorrhoids. It may vary from a slight trace of blood to considerable 
quantities. Bleeding most often occurs during defecation. Repeated 
losses of blood may occasion severe anemia. 

Hemorrhoids not infrequently affect the adjacent organs, tending 
to produce difficulty in micturition, vaginal catarrh, and possibl}^ dis- 
turbances of menstruation. 

Prognosis. — Only in conditions of great debility or because of severe 
hemorrhages do hemorrhoids endanger the life of the patient. They are 
frequently the cause of great suffering. Often they are endured for 
years before the patient seeks advice regarding them. Severe anemia 
may be caused by repeated bleedings. Sepsis or pyemia from ulceration, 
while possible, is extremely rare. 

Treatment. — The relief of constipation is of the first importance. 
The treatment of constipation must be carried out on the lines laid 
down on page 108. For the relief of hemorrhoids medicines that produce 
soft evacuations, such as salts (sodium phosphate or magnesium 
sulphate) or compound licorice powder, may be temporarily employed. 
Injections of water (Oj) or olive oil may be necessary. 

Many local measures are employed. In the milder degrees sponging 



DISEASES OF THE VEINS 



245 



the anal region with, cold water after each defecation is recommended. 
Astringent ointments, such as the ointment of galls and opium, are 
often used, but are of very doubtful value. Suppositories are much 
more effective. The best of these are anusol (iodin-resorcin sulphate of 
bismuth) suppositories. For the relief of pain suppositories of opium 
(gr. 14 to 1/2 ) or cocain gr. i/4 t)e used. Constricted or strangu- 
lated piles may be reduced by putting the patient to bed, applying ice, 
and after a time gentle pressure and manipulation as in hernia. Throm- 
bosed external piles are promptly relieved by incising them and turning 
out the clot. Whenever the distress caused by hemorrhoids or the 
bleeding is important surgical treatment should be advised. In these 
cases palliative measures are very unsatisfactory. 



DISEASES OF THE BLOOD AND DUCTLESS 

GLANDS 



ANEMIA 

Definition. — Anemia signifies a reduction either of the total quantity 
of blood or of some of its important constituents, especially hemoglobin 
and the red cells. With relation to the body anemia may be local or 
general. Local anemia will not be discussed here. General anemia is 
classified as primary or essential anemia, and secondary anemia. 
Primary anemia includes chlorosis and pernicious anemia. 

CHLOROSIS 

Definition. — An anemia of young girls, Avithout knoA\Ti cause, char- 
acterized by marked reduction of the hemoglobin. 

Etiology. — The disease affects girls usually between 14 and 17 years 
of age; recurrences develop in later years. Various causes have been 
suggested, corsets, constipation, nervous disturbances, lack of fresh air 
and exercise, all of which possibly have some slight influence but cannot 
be regarded as determinate, since cases develop under most favorable 
conditions. 

Symptoms. — General. — The patients are well nourished, the sub- 
cutaneous fat being preserved. The mucous membranes are pale, the 
skin has a pale lemon-yellow color with a tinge of green, so that the 
disease is often called the green sickness. Puffiness about the eyes and 
swelling of the ankles may suggest nephritis, while dyspnea and palpita- 
tion direct attention to the heart. Headache and neuralgia are common. 
The hands and feet are usually cold. Slight fever is not uncommon. 

Alimentary. — The appetite is capricious, often marked by a longing 
for pickles and like indigestible foods. Distress after meals and attacks 
of gastralgia are frequent. Constipation is marked. 

Circulatory. — Palpitation of the heart is often the symptom most 
complained of. Systolic murmurs over the apex of the heart and the 
pulmonic region commonly accompany anemia, especially the pulmonic. 
The heart may be slightly enlarged. The pulse is full and soft. 
Thrombosis may occur in the peripheral veins and pulmonarj^ embolism 
may result. 

Uterine. — Amenorrhea or dysmenorrhea is commonly associated. 
The function returns with improvement in the blood. 

The Blood. — In typical cases the red cells are but little reduced 
(averaging 4,000,000), but the hemoglobin is low (35-50 per cent.). The 
index is therefore lower than in any other disease. In some cases, 
however, the reduction of the red cells is more marked and the blood 
picture closely resembles that of a secondary anemia. In severe cases 
246 



DISEASES OF THE BLOOD AND DUCTLESS GLANDS 247 



the red cells are small in size and nucleated forms may appear, but 
are not common. The leukocytes may be slightly increased. The totaf 
amount of the blood plasma is increased. 

Diagnosis. — The anemia with a disproportionate loss of hemoglobin 
is characteristic. In cases resembling secondary anemia, a cause should 
be sought and pulmonary tuberculosis especially excluded. 

Treatment. — Freedom from hard work, fresh air, and good food 
are required. Iron, given in the form of Blaud's pills, containing two 
grains of sulphate of iron, is practically a specific. One, two, and finally 
three pills may be given thrice daily for many weeks. Constipation 
must be met by laxatives such as cascara sagrada or the mineral waters. 
Other disturbances are treated symptomatically. 

SECONDARY ANEMIA 

In this form the blood condition is secondary to some primary 
disease or affection. 

Etiology. — (1) Hemorrhage is one of the common causes, either 
traumatic, or resulting from gastric ulcer or cancer, cirrhosis of the 
liver, intestinal parasites, hemorrhoids, or like cause. The anemia is 
proportionate to the loss of blood. Losses of blood are quickly repaired 
by the normal organism, the serum and salts first, then the cells, and 
finally the hemoglobin. Because of this recuperative power repeated 
small hemorrhages are better borne than a single large one. (2) In- 
anition from any cause, lack of food or inability to take and digest it 
because of disease of the mouth, esophagus, stomach or intestinal 
tract, etc. 

(3) Poisoning of many kinds, by the toxins of the acute infectious 
diseases, malaria, syphilis, typhoid fever, etc., by metallic poisons, such 
as lead, mercury, arsenic, copper, etc. 

(4) The causes of anemia mig-ht be indefinitely extended, for nearly 
all the diseases included in medicine and surgery are associated, for 
one reason or another, with secondary anemia. 

Symptoms. — The general symptoms are those of primary anemia, 
pallor, weakness, headache, vertigo or syncope, palpitation, dyspnea 
on exertion, lack of appetite, constipation, and prostration of varying 
degree, dependent on the severity of the anemia. Systolic murmurs 
over the apex or the pulmonic area of the heart may be heard. 

Blood Examination. — The blood may be pale in color, or normal, 
the hemoglobin and the number of red corpuscles are reduced, but the 
reduction of hemoglobin is the greater, so that the index is below 1. 
In most cases there are but slight changes in the morphology of the 
red cells; in severe types the red cells become irregular in shape and 
size (poikilocytosis) and nucleated forms appear (normoblasts or megalo- 
blasts), but usually in small numbers. The leukocytes are usually 
slightly increased. 

In the restoration of the blood the serum and corpuscles are restored 
first, the hemoglobin but slowly returning to normal. 

Diagnosis. — The examination of the blood and a knowledge of the 



248 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



cause make diagnosis easy in most cases. From time to time cases of 
severe secondary anemia closely resembling the pernicions type are 
met with. If a cause can be found, such as pregnancy, infection by 
the hook-worm or atrophic gastritis, these cases should be classified as 
secondary anemias. 

Treatment. — Removal of the cause of anemia if possible is necessarj^ 
Otherwise the treatment must include fresh air, rest, nutritious food 
and the administration of iron, arsenic and other tonics, as in primary 
anemia, 

PERNICIOUS ANEMIA 
(Idiopathic or Progressive Pernicious Anemia) 

Definition. — A form of progressive anemia, marked at times by 
remissions, regularly fatal, characterized by an extreme reduction of 
the red blood cells and marked changes in their morphology. 

Etiology. — The exciting cause is not known. The disease has been 
observed at all ages and in both sexes, but is more commonly seen in 
middle life, and especially in men. 

Certain cases possessing the clinical characters of pernicious anemia 
and therefore often included in this categorj^ have been found to be due 
to infection with the ankylostomum duodenale or the bothriocephalus 
latus, or to follow pregnancy or parturition or cancer of the stomach. 
Although the blood picture in these cases is that of pernicious anemia, 
it would seem logical to transfer them to the class of secondary anemias, 
especially, as when the cause is recognized and removed^ the condition^ 
as a rule, is no longer either idiopathic or pernicious, but secondary and 
curable. 

Morbid Anatomy. — The skin is extremely pale, the mucous mem- 
branes blanched. The subcutaneous fat is well preserved. The body 
and organs seem almost bloodless, but little pale, Avatery fluid exuding 
from the organs. Fatty degeneration of the heart, liver, kidneys and 
other viscera is common. Much iron pigment, the result of hemolysis, 
is found in the liver cells and other organs. The spleen is small and 
atrophic. The bone-marrow changes are important. The marrow of 
long bones is red throughout. INIicroscopic examination shows 
abundance of megaloblasts and evidences of stimulation of the centers 
from which the red cells are produced. 

Symptoms. — The onset is very insidious and the disease well ad- 
vanced before the patient seeks help. Debility is the most marked symp- 
tom, usually accompanied by gastro-intestinal disturbances, nausea, 
vomiting or diarrhea. Nervous symptoms are often marked: headache 
or vertigo, somnolence, irritability, blurring of vision, or tingling in 
the hands and feet may be complained of. The patients also suffer from 
the dyspnea and palpitation which belong to any anemia. 

Fever of moderate degree may be present at times, but is rarely 
continuous. 

The pallor and debility usually increase steadily, while the gastro- 



DISEASES OF THE BLOOD AND DUCTLESS GLANDS 249 



intestinal symptoms are marked. Attacks of pain in the abdomen with 
nausea, vomiting or diarrhea are common. Minute hemorrhages into 
the retinae, skin or mucous m-embranes are common, large hemorrhages 
rare. 

Spinal disturbances are common. The reflexes are increased or di- 
minished. The gait may be ataxic or weakness may prevent walking. 
Pains referred to the feet or legs may be present. In some cases 
sphincteric control is lost. 

Periods of marked improvement are characteristic of pernicious 
anemia. These last for months or years. Death usually occurs in from 
one to three years, the fatal issue being preceded by general anasarca. 

The Blood. — The blood is very thin and watery. The red cells are 
reduced to an extreme degree, possibly less than 1,000,000. The hemo- 
globin is reduced also but not proportionately, and the index is there- 
fore 14-- The red cells show the greatest variety in form and size. 
Poikilocytes, microcytes, macrocytes, nucleated forms, both large, nor- 
mal and small (microblasts, normoblasts and megaloblasts) , may be seen. 
Variations in staining are also marked (polychromatophilia) . The leu- 
kocytes are reduced in number and the polynuclear percentage is low. 
IMyelocytes are seen at times. 

Physical examination shows the pallor, possibly with minute hemor- 
rhages in the skin, the well-preserved fat. Heart murmurs are common, 
usually systolic murmurs at the apex, or over the pulmonary valves, 
sometimes over the aortic area. Presystolic and diastolic murmurs are 
also heard at times. Unusual pulsation of the arteries of the neck or 
other parts is common. The liver may be enlarged and the subcutaneous 
glands palpable. 

Diagnosis. — The diagnosis must rest upon the blood picture, with 
the absence of any cause for anemia of severe grade. The absence of 
intestinal parasites, particularly the ankylostomum or bothriocephalus 
latus, must be established, and any other cause such as malaria, syphilis, 
cancer and the like excluded. 

Prognosis. — Recovery is possible but very rare. Periods of im- 
provement lasting for months are not uncommon. Death usually occurs 
in from one to three years. 

Treatment. — Rest, fresh air and nutritious food are most important. 
Arsenic, as Fowler's solution, is given in doses beginning with 2 drops 
and increasing to 10 or 15 three times daily. 

Systematic colon irrigation with normal salt solution has been advo- 
cated, as a remedy for a hypothetical intestinal intoxication, and has 
in some cases proven beneficial. Direct transfusion of blood may pro- 
long life for a few months w^hen other means have failed. 

LEUKEMIA 

Definition. — A disease characterized by a persistent increase in the 
. leukocytes, and associated with changes in the spleen and bone marrow 
or lymphatic glands. 



250 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



Etiology. — The disease occurs among all races and all classes, and 
at all ages, but more commonly in the years from twenty to thirty. 
Beyond these facts nothing of real value has been determined as to 
the causation of the disease. 

Morbid Anatomy. — The body is emaciated and extremely pale. 
Edema and serous effusions into the various cavities are common. 

Two varieties of leukemia are recognized according to the localiza- 
tion of the chief lesions. 

(1) Splenomyelogenous. (2) Lymphatic. It is probable that in all 
cases all the blood-making tissues are involved to some extent. 

Splenomyelogenous Leukemia. — The spleen is enormous, weights 
of 7 to 9 pounds (4,000-5,000 grams) being recorded (see Fig. 46). 
The form is preserved ; the surface is often covered by thickened whitish 
areas of perisplenitis, and adhesions are often present. The consistency 
and appearance of the section vary with the amount of fibrosis present. 

Microscopically the organ is found to be converted into tissue closely 
resembling bone marrow. In the meshes of the splenic tissue are found 
cells of the same types as those found in the blood; myelocytes abound, 
then poljTiuclear leukocytes, neutrophiies, mononuclear cells and nucle- 
ated red cells. 

Bone Marroic. — The bone marrow loses its fatty yellow appearance 
and becomes grayish-white, sometimes looking like pus. Microscopically 
myelocytes are found in abundance, numbers of non-granular mono- 
nuclears, and man}?- nucleated red cells. 

Lymphatic Nodes. — The subcutaneous lymph nodes usually show 
very slight enlargement, the intra-abdominal glands are larger. Micro- 
scopically some are normal, while others sliow more or less complete 
myeloid changes. 

The liver, lungs, kidneys and other organs are frequently greatly 
enlarged by distention of the capillaries Avith cells of the types of those 
found in such numbers in the blood. The leukemic cells are often 
massed in rounded areas which look like tumors. 

The blood presents the changes described under symptomatology. 

Lymphatic Leukemia. — The spleen is moderately enlarged and the 
bone marrow shows slight, changes. The lymph nodes, on the other hand, 
are greath^ enlarged and may form huge masses or tumors. The cer- 
vical group are usually most affected, but the axillary, inguinal, medi- 
astinal and abdominal nodes are also involved. 

Microscopically the nodes show an enormous increase in the lymphatic 
cells, and some increase in the fibrous tissue. 

The bone marrow shows a similar increase in the hTiiphoid elements, 
and lymphoid infiltration is found in the other organs, the liver and 
kidneys especially, and sometimes in such lymphatic tissues as the ton- 
sils, Peyer's patches, and the solitary follicles of the colon. 

The blood shows changes characteristic of this form. 

Symptoms. — The onset is insidious. The early complaints relate • 
(1) to the tumor in the side, the spleen. (2) To enlargement of the 



DISEASES OF THE BLOOD AND DUCTLESS GLANDS 251 



glands, especially those of the neck. (3) To anemia with its usual 
symptoms, pallor, dyspnea and palpitation. 

Some differences develop in the course of the two types. 

Splenomyelogenous Type. — Usually after the onset the disease is 
almost stationary for months. The patients are pale and feeble ; they 
lose flesh, from time to time they have fever of variable degree, but they 
complain of little except the dragging or pain due to the enlarged spleen. 

Hemorrhages from mucous membranes, the nose, mouth, lungs, 
stomach, rectum, kidney, may occur. Retinal hemorrhage may cause 
blindness. 

Gastro-intestinal disturbances, lack of appetite, nausea or vomiting, 
and constipation are common. 




\ 



\ 




Fia, 46. — The deeply-notched anterior margin of the spleen in a splenomyelogenous leukemia. 

Dyspnea and cough from leukemic infiltration of the lungs and the 
anemia are usually present. Hyclrothorax may develop. Deafness may 
be caused by leukemic infiltration of the ear or hemorrhage into it. Fever 
of varying degree may be present throughout the course. 

Finally the patients succumb to increasing anemia and feebleness, 
with edema and general anasarca. 

The Blood. — The blood is extremely pale and watery, sometimes 
suggesting pus. The leukocytes are enormously increased (100,000- 
500,000), 1:10, 1:5 or even 1:1 of the red cells. In the differential 
count a considerable percentage of myelocytes, not present in numbers 
in normal blood, is found. They may amount to 30 to 50 per cent, of 
the total count. Mast-cells are also usually present, amounting to from 
3 to 5 per cent. 




252 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



The other forms of leukocytes normally present, polynuclears, mono- 
nuclears and eosinophiles, are present in diminished percentages which, 
on account of the great total^ however, represent absolute increases in 
their numbers. 

Anemia, reduction of both red cells and hemoglobin, of the secondary 
type, is regularly present and becomes extreme toAvard the close. Nu- 
cleated red cells are usually present. 

Physical examination discloses the enormous spleen, the enlarged 
liver, some enlargement of the lymphatic glands, so that they are palpable, 
possibly tenderness over the long bones, the anemia, and in the late stages 
hydrothorax, ascites, or edema. The heart presents hemic murmurs. 
The urine shows a trace of albumin and casts, but most especially a great 
excess of uric acid due to the breaking down of leukocytes. Gravel or 
stone may result. 

The course is chronic, ranging from one to three years. 

Lymphatic Type. — The onset and course may be the same as in the 
splenomyelogenous type, but cases beginning acutely and running a 
rapid course are not uncommon. The tumors formed by the hTxiphatic 
glands are prominent features, both in the history and physical 
examination. Fever may be present as in the splenomyelogenous type. 

The Blood. — The leukocytosis is marked, but rarely as high as in 
the splenomyelogenous type, the average count being 180,000. Not in- 
frequently the counts are low — even 20,000 to 30,000! The differential 
counts show the vast majority (90-95 per cent.) of these cells to be 
lymphocytes, sometimes the large, sometimes the small forms predomi- 
nating. A few polynuclear cells are found, rarely other forms. Mast 
cells and myelocytes are rarely observed. The secondary anemia is 
present. 

Diagnosis. — The disease can be overlooked by failure to examine the 
blood. The blood examination being made, difficulty is rare. Some of 
the cases of lymphatic leukemia may for a time be confused with cases 
of acute disease accompanied by marked lymphocytosis, such as whoop- 
ing cough or miliary tuberculosis. 

Prognosis. — The disease is always fatal, but the course varies, some 
cases surviving but a few weeks, others living two or three years. 
Periods of marked improvement may occur in chronic cases. 

Treatment. — The usual hygienic and general measures for anemia 
may be employed. For the leukemia itself systematic treatment with 
X-rays by a skilled operator may produce marked improvement and in 
some cases apparent cures. The area over the spleen is usually exposed, 
but some operators also treat the epiphyses of long bones, the liver, 
or the thorax. The duration of the exposures and the intem-als 
between them vary with individual operators, so that no rules can be 
given. 

Arsenic is regularly given in increasing doses up to the toleration 
point, but is of doubtful value. 



DISEASES OF THE BLOOD AND DUCTLESS GLANDS 253 



PSEUDOLEUKEMIA 
(Hodgkin's Disease) 

Definition. — A disease characterized by progressive enlargement of 
groups of lymphatic glands and by lymphoid growths in the liver, spleen, 
lungs or other organs, without the blood changes of leukemia. 

By many the disease is regarded as a type of glandular tuberculosis, 
and in some eases tubercle bacilli have been found in the glands or their 
presence demonstrated by inoculation. On the other hand, most investi- 
gators maintain that the association with tubercle bacilli is accidental, 
that the bacilli are not to be found in many cases, and that the pa- 
thology of pseudoleukemia is definite and distinctive. 

Pseudoleukemia is also closely related, on the other hand, to sarcoma 
or malignant lymphoma of the lymphatic glands, malignant new growths 
affecting groups of lymphatic glands and producing progressive enlarge- 
ment with invasion of surrounding structures, and metastases. 

Etiology. — The disease most often attacks young persons, mostly 
males. Seventy-five per cent, of the cases occur between the ages of ten 
and forty years and but few in later life. Otherwise little of value can 
be said as to the causation. 

Morbid Anatomy. — The superficial and deep lymphatic glands are 
enlarged, usually in continuous chains. The enlarged glands form masses 
of varied size, in which, however, the individual glands are distinct; 
there is no fusion, no involvement of the capsule, no necrosis or suppura- 
tion. Pressure on surrounding structures is often manifest, the bronchi, 
veins or arteries in the chest, the ureters, veins or nerves in the lumbar 
region being affected. 

The lymphoid tissue of the tonsils and the intestines may be hyper- 
trophic. The spleen is enlarged, but not to the degree seen in leukemia. 
Lymphoid nodules are found in the spleen, liver, lungs, kidneys and 
other organs. The marrow of the long bones also shows lymphoid infil- 
tration. 

The blood shows a secondary anemia. 

Histologically the glands in many cases show a marked fibrosis with 
proliferation of the lymphoid, endothelial and reticular cells and the 
formation of giant cells, which form the picture regarded as distinctive 
by Reed, Longcope and others. Jn other cases a simple lymphoid infil- 
tration of the glands is found, and in still others tubercular lesions may 
be shown. The term pseudoleukemia must therefore still be regarded 
as a clinical term covering a group of conditions of diverse pathology. 

Symptoms. — The onset is insidious, rarely acute. (1) Enlargement 
of groups of glands, progressing in the group first involved and ex- 
tending to other groups, is usually the first symptom. (See Fig. 47.) 
The cervical are most often first affected, Init the thoracic or abdominal 
glands may be primarily involved. As the glands enlarge the tumors 
produce pressure. In the neck they may cause dilatation of the veins 
of the head and face or congestion and edema, or dyspnea or dysphagia. 



254 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



In the chest cough, dyspnea and cyanosis may result from pressure on 
the bronchi or great vessels, or paralysis of the vocal cords from involve- 
ment of the recurrent laryngeal. The growths are otherwise painless. 

(2) Anemia, slight at first, becomes marked later, and the patients 
suffer from pallor, vertigo or faintness, d^^spnea or palpitation as in any 
anemia. The blood shows a secondary anemia, without leukocytosis or 
the cell formula of leukemia. 

(3) Cachexia. — The patients lose flesh and strength and become very 
feeble. 

(4) Fever is often present either continuously or with periods of 




Fig. 47. — The enlarged cervical and axillary lymph nodes of Hodgkin's disease. From the collection 
of Dr. Walter B. James. 

normal temperature. It is usually slight and irregular, but may amount 
to a rise of several degrees daily. 

Physical examination shows: (1) The masses of enlarged glands in 
the neck, axillae, inguinal regions, abdomen or thorax. Radiographs of 
the chest are valuable aids in diagnosis (see Fig. 39). 

(2) The moderately enlarged spleen. 

(3) The secondary anemia. 

Course and Prognosis. — The disease is chronic and progressive, with 
periods of improvement in some cases. The usual duration of life is 
two to three years. Recovery under treatment is occasionally reported. 

Diagnosis. — Leukemia is excluded by the blood examination. Tuber- 



DISEASES OF THE BLOOD AND DUCTLESS GLANDS 255 



culosis must be elimininated. (1) By the examination of an excised 
gland, histologically, and for bacilli, and finally by inoculation. (2) By 
tuberculin tests, by von Pirquet's method, or by subcutaneous inocula- 
tion, if the patient is afrebrile. (3) By the absence of tuberculosis else- 
where, especially in the lungs. 

Lymphosarcoma may be confused with pseudoleukemia. The masses 
are larger in this condition, surrounding structures are invaded, metas- 
tases occur in other organs, and finally the histological examination is 
quite different. Lymphosarcoma is also much rarer than Hodgkin's 
disease. 

Treatment. — Surgical removal of the glands may relieve pressure, 
and prolong life. Repeated exposures to the X-rays may cause shrinking 
and even disappearance of local tumors. "With cessation of the treatment, 
growths reappear. 

The administration of Fowler's solution to the point of tolerance 
may also be helpful. 

PURPURA 

(Morbus Maculosus) 

Definition. — A condition characterized by the appearance of hemor- 
rhages into the skin or mucous membranes, these hemorrhages appearing 
as minute spots (petechi£e) or larger hemorrhages (vibices or ecchy- 
moses). 

Hemorrhagic eruptions belonging in this category occur symptomat- 
ically under various conditions. 

(1) In acute infectious diseases, especially small-pox, cerebrospinal 
fever, measles, septic infections, etc. 

(2) In poisoning with iodine, mercury and various other drugs. 

(3) In arteriosclerosis. 

(4) In cachectic states, such as occur in children suffering from 
gastro-intestinal diseases, in Bright 's disease, cancer, tuberculosis, severe 
anemia of any kind, etc. 

(5) In conditions putting unusual mechanical strain on the capil- 
laries, such as epilepsy or whooping cough. 

All these conditions being excluded we find purpuric eruptions occur- 
ring without apparent cause and as the prominent symptom in certain 
cases which are grouped together as purpura. 

Etiology. — Idiopathic purpura occurs at all ages, more frequently 
in males. Certain families exhibit a tendency to the affection. 

The disease is regarded by some as an acute infection. In other cases 
the condition of the blood-vessels is of primary importance. 

Symptoms. — The cases of idiopathic purpura may be grouped under 
three heads, representing different degrees of the affection. 

(1) Purpura simplex, the mildest form, seen chi(^1iy in children, and 
without the joint manifestations common in other cases. Petechial spots 
or ecchymoses appear in the skin, especially on the lower extremities, the 



256 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



patients are anemic and somewhat feeble, but otherwise feel well. A 
slight fever may accompany the eruption (see Fig. 48). 

(2) Purpura Rheumatica. — Peliosis rheumatica or Schonlein's 
disease. In this condition the purpuric eruption is associated with swell- 
ing and pain in the joints, symptoms usually wrongly regarded as indi- 
cating "rheumatism." Fever of moderate grade (102°-103°) is 
regularly present. The patients are anemic and somewhat prostrated. 

(3) Purpura Hemorrhagica. — In this form the purpuric eruption is 
accompanied by hemorrhages from the mucous membranes. Epistaxis, 
bleeding from the gums or mouth, hemoptysis, or hematemesis may oc- 
cur, or blood may appear in the stools or urine. Fever is regularly 
present, the prostration is marked, the anemia severe, and occasionally 
the disease is fatal. 

An}^ form of purpura may be accompanied by digestive disturbances, 
loss of appetite, nausea, vomiting or diarrhea, attacks of abdominal 




Fig. 48. — An extensive purpura of the legs, some fresh dark spots, others fading. 



pain. These symptoms are especially marked in the form known as 
Henoch's purpura. 

A tendency to recurrence is noted in all forms of the disease. 

Course. — This varies greatly. In the simple forms the eruption dis- 
appears in a few days. In the severer types the condition persists for 
weeks or months with recurrence of the eruption and other disturbances. 
In the severe or fulminating types of purpura death may occur. 

Complications. — Acute nephritis and cerebral hemorrhage are not 
uncommon. 

The Blood. — A secondary anemia is usually present. The blood 
platelets, which usually amount to 500,000 to 600,000 per cubic milh- 
meter, are markedly reduced, sometimes as low as 22,000. It is very 
remarkable that the coagulation time of the blood is usually normal or 
less than normal. 

Estimation of the Coagulation Time. — Various methods have been 
employed. (1) The simplest consists in putting a drop of blood 5 mm. in 
diameter on a glass slide which is kept inverted over a glass of water at 



DISEASES OF THE BLOOD AND DUCTLESS GLANDS 257 



40° C. and covered with a damp cloth. Coagulation is determined by 
turning the slide on edge from time to time and noting when the drop 
no longer sags. The normal by this method is 5 to 7 minutes. (2) 
Brodie-Russell Method. — A drop of blood on a slide is subjected to a 
stream of air blown upon it from a bulb, and the cessation of motion in 
the drop noted under the microscope. 

Diagnosis. — The cases of symptomatic purpura must be excluded, 
especially the acute infectious diseases complicated by purpuric erup- 
tions. The history of the patient and the results of physical examination 
or a few days' observation should settle the question. Cerebrospinal 
fever or malignant endocarditis or a septic infection should be especially 
looked for. 

The possibility of mistaking the bites of mosquitoes or fleas for pur- 
pura must be borne in mind. The presence of the insects, the whitish 
areola which usually surrounds bites, and the central puncture should 
distinguish them. 

Prognosis depends entirely upon the severity of the manifestations in 
the individual case. It is not often the loss of blood but the severe 
constitutional symptoms, or complicating nephritis or cerebral hemor- 
rhage which causes the fatal result. 

Treatment. — Rest in bed, fresh air and nutritious food are essentials. 
Fowler's solution is administered in increasing doses. Calcium lactate 
should be given, 15 grains thrice daily to an adult. 

In bleeding from mucous membranes, when accessible, the solution 
of adrenalin chloride 1/1000 may be applied locally, or given by mouth 
if the bleeding is from the stomach. 

In severe cases injections of normal serum, either human or animal, 
have been effective when other means had failed. The serum is given 
subcutaneously in quantities varying from 15 to 30 c.c. 

Transfusion of blood from a sound person may be tried, as a last 
resort. 

HEMOPHILIA 

Definition. — An hereditary constitutional affection characterized by 
s. tendency to severe and often uncontrollable bleedings. The hemor- 
rhages result from trivial cuts or bruises, or occur spontaneously. 

Etiology. — The affection usually manifests itself early in life, but 
may not appear till the twentieth year or even later. The tendency to 
bleed affects males particularly, but is transmitted for the most part 
through the female members of the family, many of whom are not them- 
selves bleeders. The tendency is transmitted in certain families and but 
rarely appears in others. In some of the affected families the tendency 
has been found to persist for seven generations. 

Morbid Anatomy. — No constant lesions other than the anemia pro- 
duced by bleeding can be found in fatal cases. In some patients the 
arteries have been small and thin and the tendency to bleed has been 
attributed to this condition, but it is by no means constant. The coagula- 
17 



258 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



tion time of the blood may be retarded to 45 minutes or even an hour, 
but has also been found normal in some cases. 

The theory at present accepted is that hemophilia is due to chemical 
changes in the blood and the walls of the blood vessels, owing to which 
there is a deficient production of thrombokinase, one of the essential 
elements in the process of coagulation. 

Symptoms. — The tendency to bleeding rarely appears at birth, but 
in most cases manifests itself before the end of the second year. One 
case is on record in which it first appeared in the sixtieth year. The 
bleeding may begin spontaneously, but usually follows some slight cut 
or bruise. Operations of the simplest kind, such as circumcision, may 
start it. Spontaneous bleeding may occur from the nose, mouth, stomach, 
intestines, urethra, or any other mucous membrane. Profuse uterine 
bleeding may occur in women with menstruation or after parturition, but 
this manifestation is rare. Once bleeding is begun, it may stop sponta- 
neously, or under treatment, or end only with the death of the patient. 
Profound anemia naturally occurs in those who survive attacks, and 
there is great danger of recurrence. Petechi^e, ecchymoses, or large sub- 
cutaneous hematomata may be formed. Arthritic symptoms develop in 
many cases, the larger joints becoming swollen and painful, and being 
sometimes left stiff and deformed. 

The Blood. — A secondary anemia is regularly present. There is a 
leukopenia with an increased .percentage of hTQphocytes. The coagula- 
tion time is increased, as much as an hour being sometimes required for 
clotting. 

Diagnosis. — A persistent tendency to bleeding, coupled with a family 
history of hemophilia, makes the diagnosis easy. It may be difficult or 
impossible to distinguish from chronic purpura in patients without a 
hemophilic family history. 

Prognosis. — Children showing true hemophilia rarely reach puberty. 
In older patients the prognosis is less grave. The first bleeding is rarely 
fatal. 

Treatment. — The members of hemophiliac families should be advised 
against marriage, especially the women. Children of such families should 
be protected from accident or injury so far as possible and surgical 
operations of any kind avoided. 

For the control of hemorrhage, rest, cold, pressure and the ordinary 
styptics may be tried. Calcium lactate, in doses of 1 to 2 grams (15-30 
grains) three or four times daily, is given. On mucous surfaces appli- 
cations of adrenalin chloride 1/1000 are often effective. For bleeding 
from the stomach it may be given by mouth. Applications of gauze 
soaked in a 2 to 5 per cent, sterile solution of gelatin have also proven 
serviceable. 

In intervals between bleedings, calcium lactate should be given as 
above for one or two days in each week. 

Injections of normal serum or transfusion may be employed, as for 
purpura (see p. 257). 



DISEASES OF THE BLOOD AND DUCTLESS GLANDS 259 



MORBUS MACULOSUS NEONATORUM 

Bleeding from the navel or the mucous membranes is common in 
the new-born. The hemorrhage may be associated with the jaundice of 
the new-born. It begins spontaneously during the first days of life, or 
rarely in the second or third week. In most cases the bleeding from the 
mouth, the bowel, or urinary tract goes on steadily till the child is dead. 
Spontaneous arrest may, however, occur. The measures given under 
purpura are tried, but usually without effect. In desperate cases trans- 
fusion by the direct method of Carrel has been successful. Recently 
J. E. Welch has employed Avith success the serum of normal individuals, 
giving it in doses of 10 c.c. every two hours. The reason for the effi- 
cacy of the serum is not clear; probably it supplies some element neces- 
sary to the coagulation of the blood. 

SCURVY 

Definition. — A disorder of nutrition characterized by anemia, 
debility, sponginess of the gums, and a tendency to hemorrhages into 
subcutaneous tissues or from mucous membranes. 

Etiology. — The disease appears at all ages and in both sexes. It is 
most often seen in infants fed on sterile artificial foods, or in adults 
living on a diet deficient in fresh vegetables and fresh meats. Sailors 
are therefore most often affected, but it is met with at times among the 
inmates of prisons or asylums or among the very poor. Any cause low- 
ering the vitality predisposes to the disease, especially insanitary sur- 
roundings, hard work, mental anxiety, and the like. Rarely it develops 
in healthy individuals without apparent cause. 

Theories of the Disease. — A number have been propounded. 

(1) That it is due to deficiency of potassium salts in the food and so 
in the blood. Hence the importance of fresh vegetables which are rich 
in potash salts. 

(2) That it is caused by diminished alkalinity of the blood, due to 
the withdrawal of alkaline salts from the food. 

(3) That it is caused by ptomaines developed in canned foods and 
salted meats, the usual diet of those who suffer from scurvy. 

(4) That it is a specific infection to which certain conditions, such 
as the diet and surroundings commonly associated with scurvy, 
predispose. At present no one theory has won general acceptance. 

Morbid Anatomy. — Effusions of blood into the skin, or subcutaneous 
tissues, and beneath the bones are the only constant lesions. The gums 
are swollen, soft, and possibly ulcerated. Hemorrhages may also be 
found in the serous membranes and in the joints. The blood effu- 
sions may be circumscribed or diffuse. Separation of epiphyses may 
occur in the young. Various complicating lesions, such as pneumonia, 
pleurisy, or nephritis, may be present. 

Symptoms. — Prodromal symptoms are usually observed for days or 
weeks before the appearance of the typical symptoms. The patients 



260 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



become anemic, feeble, and mentally apathetic. Gradually certain typical 
signs appear. 

(1) The gums become spongy, especially about the incisor teeth, and 
bleed easily. Ulceration may follow ; the teeth may be loosened and fall 
out. A bloody discharge from the mouth and a fetid breath accompany 
these changes. 

(2) Hemorrhages occur into the skin or subcutaneous tissue. These 
may have the usual character of petechiee, or ecchymoses, or they may 
form large hematomata, over which the skin is reddened and edematous, 
and which are very painful. As these hematomata most- often occur 
about joints, standing or walking becomes painful. 

(3) Hemorrhages from mucous surfaces, especially the nose and 
mouth, occur. 

(4) Anemia becomes marked and the patients suffer consequently 
from debility, dyspnea on exertion, palpitation of the heart, loss of appe- 
tite, and constipation. 

(5) Dysentery not infrequently results from the diet and insanitary 
conditions, and there may be blood in the stools. 

Course. — The disease, once established, continues until the condition 
is recognized and proper treatment instituted or till the death of the 
patient from exhaustion, or from complications, such as pneumonia or 
gangrene of the lung. The blood shows a secondary anemia with mod- 
erate leukocytosis. 

Diagnosis. — The conditions under which the disease develops usually 
make its recognition easy. Sporadic cases give rise to difficulty. The 
history of long-continued use of canned or preserved foods, the affection 
of the gums and the hemorrhages are characteristic. The result of 
treatment is the final test. 

Purpura or the cachexia of chronic mercurial poisoning must be 
excluded. In sporadic cases the disease is most often mistaken for some 
form of rheumatism. 

Treatment. — Removal to better hygienic conditions and a diet of 
fresh vegetables are the essentials. Fresh meat and milk are also val- 
uable. Fresh orange and lemon juice and infusions of malt are credited 
with special antiscorbutic power. The condition of the mouth must be 
treated by cleanliness and an antiseptic mouth wash of peroxide of 
hydrogen or permanganate of potash, or boric acid. 

The prevention of scurvy lies in the maintenance of hygienic 
surroundings and a dietary containing sufficient vegetable food, espe- 
cially fresh vegetables. Lime juice is given, 2 ounces per week. 

INFANTILE SCURVY 

While scurvy among the adult population has almost disappeared by 
reason of proper preventive measures, the disease has become not uncom- 
mon among infants because of the general adoption of artificial foods. 

Etiology. — A very few cases of scurvy in breast-fed children are on 



DISEASES OP THE BLOOD AND DUCTLESS GLANDS 261 



record. Sterile artificial foods, such as the proprietary cereal foods, 
condensed milk, sterilized milk, and even Pasteurized milk are the com- 
mon causes of scurvy in infants. Scurvy develops only after the infant 
has been fed for some months, as a rule, on one of these substitutes for 
breast milk, and it is therefore most often seen during the second six 
months of life, and rarely during earlier months. 

The cause of scurvy in these cases appears to be a deficiency of cer- 
tain alkaline salts, such as citrate of lime, in the food, with resulting 
diminished alkalinity of the blood, although this reduction of the alka- 
linity of the blood in scurvy has not been proven. The addition of these 
salts, in a fresh diet, or even in sterilized fruit juice, cures the disease. 

Morbid Anatomy. — Subperiosteal hemorrhages are the characteristic 
features of scurvy in infants. These hemorrhages are found on the long 
bones, just above the knee, at the ankle, wrist, or elbow. The bones may 
be rarefied and epiphyses may be separated. Hemorrhagic effusions in 
the skin, joints, or serous surfaces may also be found. The gums may 
be swollen and spongy. 

Symptoms. — The invasion is usually insidious. The children become 
fretful and cry out, when handled. They are restless and sleep poorly. 
The characteristic symptoms then appear. 

(1) Pain on any motion of the legs, so severe that the child cries out 
when touched or even approached. So carefully is voluntary motion 
avoided that the condition is sometimes mistaken for paralysis. Rheu- 
matism is the common diagnosis. 

On examination one or both legs is found swollen above the knee or 
at the ankle. The swellings are exquisitely tender. The skin is often 
glossy, possibly edematous. Instead of the legs, the arms, the ribs, or 
clavicle may be affected. 

(2) The gums about the incisor teeth are swollen, deep blue, and soft 
(spongy) so that they bleed easily. If no teeth are present the gums 
show little or no change. 

(3) Hemorrhages into the skin from mucous membranes, especially 
hematuria, may occur. 

(4) Fever of moderate degree may be present. 

(5) Rickets and scurvy are often associated, because they are both 
related to deficiency of the diet. 

Diagnosis. — Painful motion of the legs and spongy bleeding gums 
in an artificially fed child justify the diagnosis. The affection is often 
miscalled rheumatism or mistaken for paralysis or rickets. In case of 
doubt the test of a change of diet will promptly settle the question. 

Prognosis. — If the disease is recognized and properly treated, re- 
covery is wonderfully prompt and sure. Death may occur from exhaus- 
tion, bronchopneumonia or diarrhea. 

Treatment. — Sterilized or canned foods must be stopped and a 
proper dilution of fresh cow's milk or breast milk prescribed. Orange 
juice sweetened with sugar, if necessary, should be given, one or two 
teaspoonfuls thrice daily. The aff'ected liml)s should be kept as quiet ns 
possible. 



262 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



STATUS LYMPHATICUS 

Definition. — A rare constitutional condition of children or young 
adults characterized anatomically by enlargement of the thymus and a 
hypertrophy of all the lymphoid tissues, and clinically by liability to 
sudden death from trivial causes. 

Etiology. — The cause of the condition is unknown. It is closely 
associated with rickets and appears to be due to like causes, malnu- 
trition and defective hygiene. 

Morbid Anatomy. — (1) The lymph nodes throughout the body, es- 
pecially the cervical, thoracic and abdominal, are markedly enlarged; 
the tonsils, the lymphatic tissues of the nasopharynx and root of the 
tongue, solitary and agminate follicles of the intestine are hypertrophied. 
(2) The spleen is moderately enlarged. (3) The th^Tuus is enlarged 
and weighs much more than the normal organ (see Enlarged ThjTuus). 
(4) The bone-marrow shows a lymphoid hyperplasia. (5) The heart 
and aorta are often smaller than normal, the so-called hypoplasia of 
these structures. 

Diagnosis. — The subjects of this disorder are usually well-nourished, 
fat but flabby children. The enlargement of tonsils, adenoids, and the 
superficial lymphatic glands can be made out. Dulness under the manu- 
brium or skiagrams of the chest may show enlargement of the thymus 
and the mediastinal glands; the mesenteric glands may be palpable. 

Relation to Sudden Death. — Certain cases of sudden death fol- 
lowing the injection of diphtheria antitoxin, the inhalation of chloroform 
or ether, or trivial operations such as circumcision, have been found to 
be associated Avith the condition of status h^mphaticus. Death has been 
ascribed in some cases to pressure of the enlarged thjTiius gland (see 
Enlarged Thymus), but evidences of pressure are often lacking and the 
exact cause of death in these cases is not established. 

DISEASES OF THE SUPRARENAL BODIES 

ADDISON'S DISEASE 

Definition. — A constitutional disease characterized by asthenia, 
feeble circulation, gastric irritability and pigmentation of the skin. 

Etiology. — The disease is rare. JMen between tAventy and forty years 
are most often affected. Although the lesion of the adrenals is most 
often tuberculous, the disease is exceedingly rarely accompanied by CA'i- 
dences of other tuberculous lesions. 

Morbid Anatomy. — Tuberculosis of the adrenals, most often as a 
general caseation, sometimes as isolated tubercles or large tubercular 
tumors, is the most frequent lesion. Other lesions of the adrenals, cancer, 
sarcoma, gumma, etc., have also been found to cause the disease. 

Involvement of the abdominal sympathetic- has been obserA'ed and has 
been thought to account for certain cases in Avhieh the adrenals AA-ere 
normal, the nerve lesion resulting in inhibition of the function of an 
anatomically sound gland. 



DISEASES OF THE SPLEEN 



263 



Pathogenesis. — It is now generally accepted that the' disease is 
caused by an absence of an internal secretion of the adrenals, dne to 
tuberculous or other lesions, or to functional inactivity caused by lesions 
of the sympathetic nervous system. 

Symptoms. — The invasion is very insidious as a rule, the only im- 
pressive feature being increasing weakness. 

(1) The physical weakness is associated with mental apathy. Body 
and mind weary without exertion and exhaustion is produced by any 
effort. 

(2) Gastric irritability marked by loss of appetite, nausea and vomit- 
ing without sufficient cause exists throughout the disease. It shows itself 
markedly at times, with intervals when there is no disturbance. 

(3) Pigmentation of the skin is quite constant, affecting usually the 
exposed parts, the hands and face and situations like the axillae, abdomen, 
groins, or the genitals. The color of the skin varies from light yellow 
to black. It is usually progressive. Rarely it is lacking altogether. 
The buccal mucous membrane may show similar pigmented areas. 

(4) The pulse is small and very feeble, with little increase in rate. 
The blood-pressure is low. 

These symptoms constitute the essentials of the clinical picture. 

Course. — Once the disease is established it usually goes on steadily 
to a fatal conclusion, caused by syncope, or simply increasing asthenia. 
The end in most cases comes within one year, but some cases last five 
or even ten years. Recovery has taken place. 

Diagnosis. — The grouping of symptoms is characteristic, but the 
utmost care must be taken to exclude other possible causes of the 
asthenia, such as tuberculosis, cancer, myocarditis and the like. 

Tuberculin reactions should be tested for by von Pirquet's method 
or by subcutaneous inoculation. 

Treatment. — The administration of suprarenal extract should be 
tried, in tabloids of one grain, representing 15 grains of the gland, thrice 
daily. Unfortunately only a small part of the cases react favorably to 
this rational treatment. Otherwise treatment must be purely symp- 
tomatic, rest, food, fresh air, and tonics. 

DISEASES OF THE SPLEEN 

MOVABLE SPLEEN 

Etiology. — Abnormal mobility of the spleen is almost always due to 
enlargement caused by previous malaria, syphilis, tuberculosis, leukemia, 
splenic anemia or other disease. In other cases it is associated with 
enteroptosis due to congenital defects of the ligaments or relaxation 
caused by subsequent strain. 

Symptoms. — As a rule there are none. A large spleen, when dis- 
placed, may, however, cause symptoms by pressure. Pain or dragging 
may be complained of. Torsion of the pedicle may cause acute necrosis 



264 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



with intense pain, nausea, vomiting and prostration. Pressure upon the 
uterus may cause metrorrhagia. 

Diagnosis. — This must rest on the recognition of the displaced viscus, 
by its smooth external surface, general shape, and sharp, notched anterior 
border. 

Treatment. — An abdominal belt with support for the spleen may be 
effective. Opening the abdomen and packing the organ in position till 
adhesions have formed have also been successful. Removal has been done 
when other measures failed. 

RUPTURE OF THE SPLEEN 

Etiology. — Rupture occurs spontaneously or as the result of a fall 
or blow, most frequently of spleens enlarged for some reason, rarely in 
the normal organ. The symptoms are those of internal hemorrhage, 
severe pain, pallor, dyspnea or air-hunger and collapse with small, weak 
pulse. Immediate operation is demanded and usually the removal of 
the spleen. 

INFARCT AND ABSCESS OF THE SPLEEN 

Infarcts of the spleen are produced by the plugging of one of the 
branches of the splenic artery by emboli. These emboli usually come 
from the vegetations of endocarditis or the softened thrombi of pyemia 
or other acute infections, such as typhoid fever. The infarcts appear as 
pyramidal areas, deep red and firm at first, later white and fibrous. If 
produced by septic emboli they may soften or break down and form 
abscesses. The indications of infarction are pain, referred to the splenic 
region, tenderness and swelling of the spleen. A friction rub may be 
present from accompanying perisplenitis. Abscesses give the general 
symptoms of septicemia with local pain, tenderness, and enlargement of 
the organ. Peritonitis may be caused by extension or by rupture of the 
abscess. 

TUMORS OF THE SPLEEN 

Tubercles and gummata are often found post-mortem, but are rarely 
recognized clinically, owing to the greater prominence of lesions in other 
organs. Sarcoma and carcinoma as primary growths are exceedingly 
rare. Echinococcus cysts are also known. 

Amyloid spleen is present as part of an amyloid degeneration affect- 
ing also the liver and kidneys. The spleen is sometimes enormously 
enlarged. 

SPLENOMEGALY 

(Splenic Anemia. Banti's Disease) 

Under this heading are grouped several different affections charac- 
terized by marked, sometimes enormous enlargement of the spleen, and 
a secondary anemia. Several t}pes may be distinguished (Osier). 



DISEASES OF THE SPLEEN 



265 



(1) Simple splenomegaly, in which the spleen is greatly enlarged 
with little or no anemia and only slight dragging or pain from the 
weight of the organ (see Fig. 49). 

(2) Splenomegaly with marked secondary anemia, a tendency to 
hemorrhages, and pigmentation of the skin. The hemorrhages occur 
from various mucous membranes, especially the stomach. Cirrhosis of 
the liver with ascites may develop in the final stages (Banti's disease). 
These conditions persist for many years. 

(3) A family or infantile type, which begins in childhood and in 
many cases affects several members of a family. Cirrhosis of the liver, 
jaundice, pigmentation of the skin and stunting of the growth of the 




Fig. 49.- Splenic anemia: the lines mark the edges of liver and spleen. 

children have been observed. In some cases a simple fibrosis of the 
sp^^een is present, in others a very remarkable endothelial hyperplasia 
involving not only the spleen, but the liver, lympli nodes and the medulla 
of the bones. Various names have been given to the condition, endo- 
thelioma, chronic endothelial hyperplasia, Gaucher 's type of spleno- 
megaly, etc. 

The diagnosis of these conditions rests upon the associated enlarge- 
ment of the spleen and ^inemia, in the absence of any of the usunl causes 
for chronic splenic enlargement, such as rickets, syphilis, tuberculosis, 
malaria, leukemia, Tlodgkin's disease, or chronic polycythemia, etc. 

Treatment of the anemia and exposure to the X-rays have given 
some relief. Splenectomy has been successful in a few cases. 



266 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



POLYCYTHEMIA 
(Erythrocytosis Megalosplenica) 

Definition. — A rare disease cliaracterized by cyanosis, increase in the 
number of red corpuscles per cnbic millimeter of blood and enlargement 
of the spleen. 




Fig. 50. — Polycythemia with cyanosis (of the face and hands). The margrins of enlarged spleen and 
liver marked on the abdomen. From the coUectioji of Dr. A. R. James. 

Etiology. — The cases thus far reported include both men and women 
from 35 to 60 years of age. 

Symptoms. — The patients complain of headache, vertigo or weakness. 
Sometimes the color of the skin and mucous membranes excites concern. 
This color is a deep bluish-red, the lips and finger-nails look blue, as in 
cyanosis (see Fig. 50). Hemorrhages from the mucous membranes, neu- 
ralgia, dyspnea and edema of the lungs have been observed. Temporary 
improvement may occur, but the disease persists indefinitely. 



DISEASES OF THE THYROID GLAND • 267 



Examination shows an enlarged, often an enormous, spleen and the 
polycythemia. The red cells exceed 8,000,000 and may number 13,000,000 
per c.mm. The hemoglobin varies from 120 to 190 per cent., and the 
leukocytes are increased, with a relative increase of the polynuclears, 
even to 92 per cent. 

Treatment. — Bleeding gives temporary relief. X-ray treatment re- 
duces the spleen and the number of red cells. 

DISEASES OF THE THYROID GLAND 

CONGESTION 

Congestion of the thyroid is especially associated with changes in 
the menstrual function, so that it appears at puberty, with the menstrual 
period and, it is said, with defloration. It may also be produced by 
tight collars, prolonged crying, epileptic fits and the like. Beyond the 
swelling no symptoms are produced and the condition is transient. 

ACUTE THYROIDITIS 

Acute inflammation of the thyroid occurs as (1) the result of the 
action of certain poisons, such as alcohol, iodine or phosphorus, or (2) 
as a complication of acute infectious diseases, such as typhoid and 
scarlet fever, measles, small-pox, etc. The inflammatory process may 
be simple or suppurative. In the suppurative cases various organisms, 
staphylococci, streptococci, the typhoid bacillus, etc., have been re- 
covered. 

Symptoms.— The gland is swollen, and in the severer cases tender. 
Usually one lobe is the more affected. In suppurative cases, the skin 
becomes reddened and fluctuation develops. The enlarged gland may 
give the usual signs of pressure, congestion of the neck and face, 
dyspnea or dysphagia. Graves' disease or myxedema may follow. 

Treatment. — A light ice-bag may be applied and rest enjoined. 
Suppurative conditions must be promptly opened. 

GOITRE 

Definition. — A chronic hypertrophy of the thyroid gland. 

Etiology. — The affection occurs sporadically and endemically. 
Sporadic cases occur in women in all parts of this country^ The disease 
is endemic in certain mountainous regions, especially Switzerland and 
parts of France, also in South America and Asia. In Switzerland 
especially goitre is frequently associated with cretinism. The drinking 
water is usually regarded as the cause of the affection. 

In North America endemic centers have been found in regions at 
the eastern end of Lake Ontario, in Michigan and the mountainous 
parts of Pennsylvania. Epidemics have been observed in schools and 
garrisons. 



26« DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



Morbid Anatomy. — In general there is an increase in all parts of 
the gland. Certain varieties are named from the predominant features 
of the process. (1) Parenchymatous, when the glandular structure 
is most hypertrophied, the enlarged follicles being filled with normal 
colloid material. (2) Cystic, when the follicles are so much enlarged 
as to give the impression of cysts. These cysts may be formed by 
enlargement of a single follicle or the fusion of several. (3) Vascular, 
when the vessels are notably dilated. The enlarged vessels frequently 
show atheromatous changes. (4) Fibrous, when the interstitial tissue 
is greatly increased and the gland is firm or hard. 

Symptoms. — The whole gland may be uniformly enlarged or only one 
lobe, especially the right. The enlargement may be slight or extreme 
in degree. Symptoms consist only of the appearance of the tumor and 
pressure if it be large. Dyspnea from pressure on the trachea, rarely 
dysphagia from obstruction of the esophagus, congestion of the head 
and neck from pressure on veins, and disturbance of the heart from 
pressure on the pneumogastric nerves may result. 

The growth is painless, and is soft, cystic, or hard, according to the 
degree of involvement of the several parts of the gland. Pulsation may 
be felt and a systolic murmur heard in cases of vascular goitre. 

Diagnosis. — Goitre is distinguished by the characters of the tumor 
and the absence of the sjonptoms observed in Graves' disease. The 
tumor moves upward in deglutition. 

Prognosis is good as to life. Sudden death may occur from tracheal 
stenosis, disturbance of the heart, edema of the glottis or apoplexy, but 
is rare. 

Treatment. — Removal from a goitrous district and the boiling of 
drinking water are employed as prophylactic measures. Iodine is given 
either as potassium iodide, 5 to 10 grains thrice daily, or 1 dram of the 
liquor iodi compositus. Excessive dosage may cause symptoms resem- 
bling Graves' disease, nervousness, palpitation, sweating, tremor, etc. 
X-ray treatment has also been effective. Surgical measures may be re- 
quired for relief of pressure. 

TUMORS OF THE THYROID 

Adenoma, simple or malignant, sarcoma and cancer are known, but 
are very rare in comparison vrith the common goitre. These tumors 
have their usual characters. SjTuptoms are due chiefly to pressure. 
Treatment is surgical. 

EXOPHTHALMIC GOITRE 
(Graves' Disease. Basedow's Disease) 

Definition. — A disease due to morbid function of the thyroid and 
characterized by exophthalmos, goitre, tachycardia, and tremor, or Iw 
any combination of these cardinal symptoms. 

Etiology. — Women are more affected in the proportion of 6 or 8 



DISEASES OF THE THYROID GLAND 



269 



to 1. The disease usually appears between the ages of 16 and 40. 
Beyond these facts little of value is known concerning- the causation of 
the disease. 

Fright or protracted worry is found to precede the onset in some 
cases, in others some acute infection, such as tonsillitis, and in still 
others intestinal disturbances, but the influence of these factors is not 
marked. 

Moebius' view that exophthalmic goitre is an intoxication due to 
morbid function of the thyroid gland is now generally accepted. The 
antithesis to myxedema presented by exophthalmic goitre is striking. 
The results of the administration of excessive doses of thyroid gland 
are also very suggestive of exophthalmic goitre. Even the exophthalmos 
has been produced in this way. It is, however, clear that exophthalmic 




Fig .51. — Exophthalmic goitre: showing the exophthalmos and the goitre. 

goitre is due not alone to excessive functioning of the gland, but also 
to abnormal secretion. 

Morbid Anatomy. — The thyroid gland is usually enlarged, but may 
be smaller than normal. The gland shows a diffuse fibrosis, with marked 
changes in the epithelium of the alveoli. The colloid is diminished or 
increased in amount and altered in quality. Whether these changes are 
peculiar to exophthalmic goitre is an open question. 

The thymus is often persistent and enlarged. There are no other 
constant lesions. 

Symptoms. — (1) Goitre of some kind is present in nearly all cases, 
but may be entirely lacking. The enlargement of the gland may be 
of any degree or type. Thus the gland is but slightly enlarged in 
some ca^es, quite large in others. The whole gland may be affected or 
only one lobe. The goitre may be soft and elastic or cystic, but is 
more often firm or hard. A thrill and a systolic, a diastolic, or a con- 
tinuous murmur may be heard over the gland (see Fig. 51). 



270 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



(2) Tachycardia with other symptoms of vascular excitation is 
"usually present. The pulse rate varies from normal to 200 or more. 
Palpitation and dyspnea on exertion usually accompany the tachy- 
cardia. 

The patients may also complain of the throbbing of the arteries 
in various parts of the body. Late in the disease the pulse often be- 
comes slow and intermittent. 

The heart is slightly enlarged, its impulse very forcible, and the 
shock of the heart sounds palpable. The throbbing of the carotids, the 
abdominal aorta and even the peripheral vessels is marked. The capil- 




FiG. 52. — Graves' disease, showing the emaciatinn, exophthalmos, and goitre. 

lary pulse or throbbing in the veins of the hand may be observed. 
Flushing of the face or other parts of the body is common. 

On auscultation cardiac murmurs are usually heard, systolic mur- 
murs at both base and apex, and loud, sharp heart sounds. The pulse 
often has the Corrigan quality. 

(3) Exophthalmos — protrusion of the eyes — is usually present. The 
causes of this symptom are still in doubt. Cong^estion of the orbital 
vessels, increase of orbital fat, edema, and spasm of the special orbital 
muscle of Mueller have all been suggested. The ocular sjmiptoms of 
the disease have been given the names of different observers. 

The staring with diminished frequency of winking is kno^Mi as 
Stell wag's sign. 

Graefe's sign consists in failure of the upper lid to follow smoothly 



DISEASES OF THE THYROID GLAND 



271 



a downward motion of the eyeball. The lid lags behind or even jerks 
backward. 

Moebius' Sign. — In near convergence of the eyes, as in fixing the 
eyes on the tip of the nose, one eye will turn outward, owing to muscular 
weakness. 

Because of the diminished motion of the lids and loss of sensitive- 
ness in the cornea, conjunctivitis or ulceration of the cornea may result 
in advanced cases. 

(4) Tremor. — A rapid fine tremor is present in the fingers and 
possibly the tongue. Associated with this tremor are various nervous 
symptoms, including mental excitability, irritability or restlessness. 
Mental depression or exaltation may occur. 

(5) Various other symptoms are more or less commonly met with. 
Emaciation is frequent (see Fig. 52), especially late in the disease, and 
persistent diarrhea is common. Fever is present in many cases, very 
irregular in its daily and weekly variations. 

Course. — The evolution of the symptoms may be rapid or slow. 
Once the disease is established the course is chronic, usually lasting for 
years. 

Recovery is not uncommon under treatment, either medical or 
surgical. Death may result, either from the disease itself or com- 
plications, such as pneumonia or tuberculosis. 

Diagnosis. — Fully developed cases can hardly be mistaken. With 
one or more of the cardinal symptoms missing, doubts arise and 
opinions differ. 

Treatment. — (1) Symptomatic— Rest, both physical and mental, is 
necessary from the outset. Many remedies have been advised and used. 
Digitalis or strophanthus to slow the pulse, belladonna and ergot to 
control the vascular disturbances, phosphate of soda and intestinal 
antiseptics to meet the assumed intestinal autointoxication. 

(2) Organotherapy. — Various preparations made from the blood, 
the serum, or the milk of thyroidectomized sheep or goats are in use. 
The serum of rabbits treated by injection of the nucleo-proteid or 
thyroglobulin of the thyroids obtained from cases of Graves' disease 
has also been used with some success. 

(3) Electricity and the X-rays have relieved or cured some cases. 

(4) Surgical treatment is increasingly successful and should be 
advised after reasonable trial of other methods. The ligation of the 
superior thyroid arteries or removal of part of the gland is usually 
recommended. 

MYXEDEMA 

Definition. — A disease caused by loss of function of the thyroid 
gland, and characterized by atrophy of the gland, mental hebetude, and 
a myxedematous condition of the subcutaneous tissues. 

The condition may be due to con (genital defect of the gland (cretin- 
ism), or to loss of function in adult life (myxedema) or the operative 
removal of the gland (operative myxedema). 



272 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



CRETIXISM 

Etiology. — Cretinism occurs in both endemic and sporadic types. 
The endemic type is common in the mountainous regions of Switzerland, 
France and Italy. The sporadic cases are found under any conditions. 
Since the recognition of the disease many cases have been discovered 
in America. 

Symptoms. — During the second six months of the child's life it is 
noted that dentition is delayed and that the cliild does not develop 
mentally. During the second year the typical features of cretinism 
appear. The form is stunted, the limbs short and thick. The hair is 
thin and dry. The tongue is thick and often protrudes from the mouth. 




Fig. 53. — A cretin aged 25 years. Xotethe shrunken figure, expressionless face, protuberant abdo- 
men with umbilical hernia, and kyphosis. 

Fig. 54. — The same cretin, dorsal view, showing the lateral curvature of the spine. 

From the collection of Dr. W. P. Northrup. 

The face is expressionless, the eyes dull, the skin thick. The teeth, if 
present, decay early (see Figs. 53 and 54). Over the clavicles there are 
pads of myxedematous tissue. The body is heavy, the abdomen prom- 
inent, and umbilical hernia is common. The muscles are weak. The 
child walks late, talks late, and remains mentally undeveloped, an. 
idiot or imbecile in many cases. The temperature is subnormal, the 
pulse slow. Unless relieved by treatment these characters persist into 
adult life, and from time to time typical cretins of 30 or 35 years are 
discovered. 

myxede:\l\ 

Etiology. — Myxedema affects women in the ratio of 6 to 1. Goitre 
or Graves' disease may precede it. The tendency to myxedema is trans- 
mitted in some families. 

The symptoms are ver\^ like those of cretinism. Increasing mental 



DISEASES OF THE THYROID GLAND 



273 



dulness is usually first noted, then the hair becomes thin and dry, 
the skin pale, sallow, dry and thick, especially in the face and extremities, 




Fig. 55. — Myxedema, showing the thin, dry hair, the puffy eyelids, and the dull, heavy expression 

of the face. 

so that the patients are often thought to have nephritis. The tongue 
grows thick, the speech slow and scanning and very limited. The nose 



Fig. 56. — Myxedema. The backs of the hands are puffy, the skin dry, wrinkled, parchment-like. 

becomes broad and thick (see Figs. 55 and 56). The bodily movements 
become slow and heavy. Memory fails and often the patients become 
18 



274 DISEASES OF THE BLOOD AND DUCTLESS GLANDS 



irritable or suspicious. Dementia may result. The temperatui^e may 
be below normal and the pulse slow. 

Operative myxedema or cachexia strumipriva was not uncommon 
foUo^nng complete removal of the thyroid giand for goitre or other 
cause, but now is rarely seen since only partial removals are attempted. 
The symptoms are those of myxedema. 

Diagnosis. — The diagnosis of cretinism is extremely easy, if one 
has the condition in mind. Xo other congenital defect closely resembles 
it. In mild cases doubt may arise. Treatment may then be tried 
experimentally. 

Myxedema has often been mistaken for Bright 's disease because of 
the swollen face and extremities and the presence of albumin and casts 
in the urine, a common finding. The mental dulness, the condition of 
the hair, and other features named should distinguish it. 

Treatment. — The thyroid giand of the sheep is administered in 
tablets. For a child, 1/5 to 1/4 grain may be given thrice daily, for an 
adult 1 grain. The dose is then increased gradually to 10 or 12 times these 
amounts. Treatment may be stopped from time to time and renewed 
again. The results are often marvelous. In rare cases the treatment 
has no effect. The administration of too large doses of the thyroid gland 
produces fever, restlessness, rapid pulse, and prostration. 

DISEASES OF THE THYMUS GLAND 

Interest centers in the persistence and hypertrophy of the gland. 
The old teaching that the giand normally atrophies after the second year 
is incorrect. A table, prepared by Nicoll and the writer, of the weights 
of 495 glands from children varjang in age from birth to five years 
showed the weight of the gland to average practically the same through- 
out that period. Cunningham, of Edinburgh, states that the gland regu- 
larly persists, but is lost to observation in the increasing mediastinal 
fat. L'^nder certain conditions, however, the gland is found much in- 
creased in size. 

Hypertrophy of the thjTnus is associated, as a rule, ^^ith a general 
hypertrophy of the hTnphoid tissues (see Status L^Tnphaticus). Occa- 
sionally the hypertrophy of the giand is so great as to dominate the 
picture. Ever since the appearance of Friedleben's great monograph 
on the Th^Ttius in 1858, discussion has been carried on regarding the 
possible relation of enlargement of the th^^nus to larj^ngismus stridulus 
or other dyspnea produced by pressure on the trachea, the so-called 
thymic asthma. Friedleben denied the influence of the tliATQus. others 
have affirmed it and the discussion is still open. The relation of enlarge- 
ment of the thymus to sudden death is also still under discussion. (See 
p. 262.) 



VI 

CONSTITUTIONAL DISEASES 



CHRONIC POLYARTHRITIS 

Definition. — A constitutional disease characterized by chronic in- 
flammation of a number of joints, anemia and malnutrition, the etiology 
of which is unknown. 

Chronic polyarthritis may arise from a niunber of causes, some 
undoubtedly bacterial, as gonorrheal, tubercular, pneumococcic, or septic 
infections; some metabolic, such as gout and the purpuric affections; 
some of nervous origin, such as those occurring in syringomyelia, and 
locomotor ataxia. When all these groups have been separated off, there 
remains a considerable number of cases of chronic polyarthritis for 
which no satisfactory explanation can at present be given. For some 
years efforts have been made to classify these cases, as hypertrophic 
or atrophic or periarticular, according to the nature of the changes 
observed in the affected joints. No good result has been reached in 
this way, and the procedure is no more satisfactory than would be the 
division of tubercular arthritis on a like basis. It therefore seems best 
at this time to include all these cases under one broad term, substituted 
for the designation of Arthritis Deformans, which is applicable only 
to one of the several groups into which these cases readily fall when 
classified on anatomical grounds. It will be noted that chronic rheumatism 
is included. The term rheumatism in this connection no longer has any 
clear meaning and should be dropped. 

Etiology. — The conditions under which chronic polyarthritis is met 
with may be stated, although they throw practically no light on the 
real cause of the disease. Children are but rarely affected. Adults of 
all ages and both sexes suffer from it. Elaborate studies of the age, 
race, sex, social condition, employment, and previous illnesses of patients 
have been productive of nothing of value. The metabolism of the 
patients has been studied, especially the nitrogenous metabolism, without 
result. In some studies the calcium and magnesium metabolism has 
been investigated, with the result that some cases show retention, others 
loss of these substances so closely related to bone formation. As stated 
in the definition the etiology of these cases is unknown. 

Morbid Anatomy. — There is a chronic inflammation of a number 
of joints, usually symmetrically placed, and either large, such as the 
ankle, knee, or hip, or small, such as the finger-joints. The affected 
joints are large, either partly or completely ankylosed, the tissues about 
them are dense. The muscles of the part are atrophied, both above and 
below the joint. The skin is often dry and glossy and cracks easily. 
If the joints are opened, the secretion is found either increased or 
diminished. The synovial membranes are thickened. The cartilages are 

275 



276 



CONSTITUTIONAL DISEASES 



fibrillated and often eroded. The capsule is thickened and dense. The 
articular ends of the bones are thickened, or atrophied, or in some cases 
exposed in the joint and ebumated. The periarticular tissues are much 
thickened and adherent, tendons about the joint being firmly bound 
down. 

According to the degree in which the several parts of the joints 
are affected in different cases the lesions have been classified as (1) 
Hypertrophic — in which new bone has been formed about the joints, 
producing the so-called osteophytes. As a result of new formation of 
bone at one point and erosion at another the joints are greatly deformed 
(arthritis deformans). (2) Atrophic — in which there is rarefaction of 
the articular ends of the bones forming the joints and atrophy of other 
tissues, so that the joints may seem smaller than normal. (3) Peri- 
articular — the chief lesion being found about rather than in the joint, 
the periarticular tissues being swollen, thickened, and densely adherent. 
This is the most common form and is usually denominated rheumatoid 
arthritis- 
Symptoms. — 1. Monarticular Type. — A number of joints are 
usually affected in some degree, but the process becomes so marked 
in a single large joint, the hip, knee, or shoulder, that it dominates 
the picture. The joint is painful, especially on motion, enlarged and de- 
formed, and motion becomes progressively restricted. The muscles above 
and below the joint atrophy. From time to time the pain and restriction 
of motion are aggravated. The condition is very chronic and may result 
in complete ankylosis (see Fig. 40). 2. Vertebral Type: The joints 
of the spinal column are involved, sometimes in part, sometimes through- 
out. Pain and limitation of motion are the marked features, the spine 
becoming more or less rigid (poker back). Pain is felt in the back or, 
if intercostal nerves are involved, referred to the chest or abdomen. 
As in the other forms, the disease is chronic and progressive and the 
disability resulting may be severe. The general health may suffer 
from the constant pain. 3. Heberden's Nodes : The joints of the fingers, 
especially the terminal phalanges, are involved in this type, often without 
participation of other joints. The articular ends of the bones are 
roughly enlarged by exostoses, the joints suffer to some extent, with 
pain and limitation of motion, and sometimes marked deformity from 
deflection of the terminal phalanges. Exacerbations occur as in other 
types. Often no other symptoms are complained of and the patients 
think little of the slight deformity and disability. 4. General 
Progressive Type: An acute and chronic form are described, (a) 
The acute type closely resembles the milder attacks of rheumatic fever. 
A number of joints are swollen, tender, and painful, and the patients 
suffer from fever and become anemic as in rheumatic fever. These 
attacks are regularly mistaken for rheumatic fever. The joint lesions 
are not so red, or so exquisitely tender as in the later affection, they 
do not yield to the salicyhiti^s, but persist and deveU^p characteristic 
lesions of the bones and joints, (b) Chronic type. In tliis form one 



CHRONIC POLYARTHRITIS 



277 



joint after another is involved by a chronic progressive arthritis which 
produces swelling, pain, and limitation of motion (see Fig. 57). The 
disease may progress from one joint to another of the body till all are 
ankylosed to a greater or less degree (see Fig. 58). From time to time 
the joint symptoms are intensified, and the temperature is raised as in an 
acute attack. The patients suffer from impaired digestion and become 
anemic, and the muscular atrophy about the affected joints may be ex- 
treme. In its severe form the disease reduces the patient to a helpless 
invalidism. The blood shows the changes of a secondary anemia. 

Diagnosis.— The diagnosis of chronic polyarthritis or arthritis de- 
formans implies the exclusion of all the known causes of such con- 




FiG. 57. — Chronic polyarthritis. Arthritis deformans: showing the enlargement and deformity of 

the joints of the wrists and fingers. 

ditions. Rheumatic fever can easily be confused with the first acute 
attacks of the general progressive type. Failure of the salicylates to 
produce any effect on the process is suggestive. The cardiac complica- 
tions, involvement of the pleura and pericardium belong to acute 
rheumatic fever, and not to chronic polyarthritis. The after course of 
the affection makes the differentiation easy, as chronic polyarthritis 
tends to persist and produces progressive changes. Gonorrheal arthritis 
must be excluded by a knowledge of the history, examination of the 
urethra or vagina for gonococci, or the fluid of joints, if effusions are 
present. Sometimes a therapeutic test of the influence of gonococcus 
serum or vaccines is indicated. Tuberculosis must be excluded by a 
study of the lesions, the absence of any tendency to the formation of 



278 



CONSTITUTlOXAIi DISEASES 



pus or discharging sinuses in chronic poh^arthritis, and in some cases by 
Yon Pirquet's test or the snbcutaneons inocnlation of tuberculin. Sep- 
tic arthritis can be excluded only by the clinical history, the absence of 
any preceding disease such as scarlet fever, pneumonia, or endometritis. 
Skiagraphs constitute a most valuable aid in determining the nature and 
extent of the changes in and about the joints. 

Prognosis. — This varies to some extent in the different types of the 
disease. The monarticular type tends to disablement of the .joint most 
involved, but the general health suffers little. Heberden's nodes, as a 
rule, affect the life and comfort of the patient hardly at all. The 
progressive type is severe and, while the disease is not fatal, tends to 




Fig. 58. — Case of arthritis deformans from Dr. Young's clinic. (International Clinics, 
Vol. Ill, Series 20.)- 

permanently cripple the patient and possibly renders him quite helpless. 
Death results from intercurrent disease. 

Treatment. — Medicines have no specific effect upon the condition. 
Treatment must be hygienic and dietetic. Eesidence in a dry, mild 
climate is desirable. The diet must be suited to the digestive capacity 
of the patient and must be as nutritious as possible. Restriction of 
proteid food such as is practiced in gout is not beneficial. Abundance 
of fat in the form of butter and cream is indicated. The patients must 
be encouraged to take such exercise as is possible without severe pain. 
Continued inactivity tends to increase the disability. For the arthritis 
rest and immobilization should be practiced only in the acute exacerba- 
tions and then for a limited time. Hydrotherapy is employed in various 
forms. Alternate applications of hot and cold water, or hot and cold 
douches, to the affected joints, are often beneficial. The hot-air treat- 



MUSCULAR RHEUMATISM 



279 



ment, baking the joints for 10 to 15 minutes in dry air at a temperature 
of 250° to 300° or even more, is often employed. Electric-light baths, 
either local or general, have a similar effect. Massage with passive 
movements of the joints is helpful in preventing muscular atrophy and 
maintaining the motion of affected joints. 

MUSCULAR RHEUMATISM 
(Myalgia) 

Definition. — An affection characterized by pain in certain groups 
of muscles. In its literal meaning the term is often used to cover any 
muscle pain. Clinically its application is limited to pains in muscles 
not accounted for by neuritis, by the presence of parasites (trichina), 
or by trauma, or tumor or other definite lesion. According to the 
muscles involved the disease is termed torticollis (muscles of the neck), 
pleurodynia (the intercostals) , lumbago (muscles of the back), scapu- 
lodynia (muscles of the shoulder), etc. 

Etiology. — The causes commonly include: (1) Exposure to wet or 
cold. (2) Trauma. (3) A rheumatic or gouty diathesis. 

Morbid Anatomy. — The affection was long regarded as a neuralgia 
without definite anatomic lesions. Later it was supposed to be a 
myositis. Recent studies have shown the only definite lesions to be in 
the white fibrous tissue sheathing the muscles and nerves, and forming 
tendons and periosteum. The lesions found were swelling, edema and 
degeneration of the fibrous tissue. 

Symptoms. — Pain is the one constant symptom. It may be acute 
and sharp or a dull aching. It is regularly aggravated by motion and 
relieved by rest. Usually it comes and goes in varying severity. An 
attack u.sually lasts from a day or two to a week. In some cases the 
condition becomes chronic. Recurrences are frequent. Torticollis derives 
its name from the fact that with the pain the head is turned to 
one side by contraction of the affected muscles. Lumbago may also 
show contraction of the muscles involved. On examination the muscles 
may be found tender to pressure, motion aggravates the pain, and in 
some cases definite nodules may be found in the muscles. These nodules 
are small indurated areas, feeling like shot imbedded in the tissues. 

Treatment. — Rest for the affected muscles is of first importance. 
This is secured by strapping the lumbar or intercostal regions, or by 
rest in bed in severe cases. Counter-irritation with the Pacquelin 
cautery is often helpful. Heat in other forms (the hot water bottle 
or electric light) may be employed. Acupuncture has been successful 
in lumbago. Of medicines sodium salicylate, gr. x-xv, every 3 or 
4 hours, or aspirin, gr. x, may be given. Colchicum has better effects 
in some cases. The chronic or recurrent cases are treated for a gouty 
diathesis by reduction of proteid food, the free drinking of water, 
regulated exercise, and hydrotherapy, hot baths and packs. 



280 



CONSTITUTIONAL DISEASES 



GOUT 
(Podagra) 

Definition. — A disorder produced by defective nitrogen metabolism 
and characterized by excess of uric acid in the blood and recurrent 
attacks of arthritis due to the deposition of sodium biurate. 

Etiology. — A number of factors are active in most cases, such as 
(1) Heredity. The disease or tendency to it may be marked in successive 
generations of a family, doubtless from like habits of living. (2) The 
excessive use of alcohol, especially in the fermented beverages, such as 
wines, beer and ale. The distilled liquors, whiskey, rum. and gin, appear 
less harmful. (3) Overfeeding, especially if the diet be over-rich in 
meat or other nitrogenous foods. (4) Deficient exercise. Lack of proper 
relation between food and exercise is the more accurate explanation of 
overfeeding. (5) Lead-poisoning is. in England, a frequent antecedent. 
Apparently it is less frequently seen in this country. 

Morbid Anatomy. — The blood. An excess of uric acid may be 
demonstrated by Garrod's thread test. To 2 drams of serum, taken 
either from the drawn blood or from a blister, 6 minims of moderately 
strong acetic acid are added in a flat water crystal. A fiber or two of 
Imen thread is then introduced and the preparation set aside for from 
36 to 60 hours. If uric acid is present in excess it will be found in 
crystals upon the thi-ead. The test often fails. 

The Joints. — The affected joints are enlarged, the periarticular tis- 
sues thickened, and deposits of sodium biurate in the form of tophi are 
present in the cartilages of the joints and in the periarticular tissues. 
The tophi sometimes form masses of considerable size about the joints, 
or there may be only small nodules. When opened, the tophi are found 
to contain a thick, paste-like material, which has been sho\^'n to be mainly 
sodium biurate. The cartilages of the involved joints may be eroded in 
advanced cases. Tophi or chalk-stones are also found in the lobes of 
the ears, in the tendons and subcutaneous tissues, rarely in the lar^Tigeal 
cartilages or cords and other sites. 

The ASSOCIATED LESIONS of gout are found in the kidneys, heart, and 
arteries. The kidneys show the lesions of chronic interstitial nephritis, 
commonly in the form of contracted kidney, in other cases the larger, 
hard, red kidney of arteriosclerosis. The arteries, both the aorta and 
the peripheral vessels, present a marked condition of arteriosclerosis. 
The heart shows hypertrophy of the left ventricle, frequently accom- 
panied by sclerosis of the coronary arteries and myocarditis or fatty 
degeneration of the heart muscle. Pericarditis may be found. 

Chemistry of Gout. — As the result of clinical study and experimental 
investigation, the following propositions may be said to be fairly estab- 
lished. Gout is due to a disturbance of the nitrogenous metabolism of 
the body. The blood in gout is found to contain an excess of uric acid. 
This uric acid is derived mainly from the breaking down of nucleo- 
proteids of the cells either of the body itself or of the food, and accord- 



GOUT 



281 



ing to its source the uric acid is tlierefore designated as endogenous or 
exogenous. A part of the endogenous uric acid has been shown to be a 
product of muscle metabolism. According to the generally accepted 
theory of Emil Fischer the nuclein or nucleic acid of cell nuclei contains 
a hypothetical base called by him purin. Uric acid and the so-called 
xanthin or purin bases (xanthin, hypoxanthin, guanin and adenin) 
are all derived from this hypothetical substance by a process of oxida- 
tion. This oxidation is brought about not by the simple step of chemical 
combination, but through the intervention of certain ferments. These 
ferments are not uniformly present in all the fluids or tissues of the 
body, but are found especially in the pancreas, adrenals, thymus, and 
spleen. Similarly the final step in the transformation of uric acid into 
urea is brought about by a special ferment shown to be present in the 
liver, muscles, kidneys, and bone-marrow. In the light of present evi- 
dence it seems probable that the defective nitrogenous metabolism char- 
acteristic of gout is brought about either by the absence or inhibition 
of this ferment called oxidase, which has the power of oxidizing and so 
converting uric acid into urea and other products. 

Symptoms. — Acute Gout. — The onset is sudden with severe pain 
in one joint, usually the metatarso-phalangeal of one or the other great 
toe. The joint is swollen, red and very tender. The temperature rises 
to 101° or 103°. The patient's suffering is intense. With the morning 
the pain and fever subside, usually to recur the following evening for 
a week or ten days. The inflammation then subsides and the patient 
is well for an indefinite time ; sooner or later the attack is repeated. 
Other joints than that of the great toe, especially the tarsal, may be first 
affected. Chronic Gout. — With repeated attacks other joints become 
involved, the tarsus, ankle, knee, wist, or elbow% rarely the hip, or 
shoulder. Recurrences, much like acute attacks, become frequent. The 
affected joints become thickened, stiff, and studded with tophi of varying 
size. The tophi sometimes form tumors of considerable size, and may 
ulcerate and discharge their thick, paste-like contents, which on micro- 
scopic examination show crystals of sodium biurate. Tophi may also 
appear in the cartilages of the ears or in tendons, the subcutaneous 
tissues, or even in the larynx, etc. Gradually the arteries thicken, the 
heart hypertrophies, and the urine presents the changes of chronic inter- 
stitial nephritis. The course of the disease is exceedingly chronic, the 
attacks of arthritis being separated by long intervals of comparative 
comfort or illness due to some of the complicating conditions. The 
patients are also likely to suffer from chronic bronchitis and emphysema. 
The fatal termination is usually brought about by an attack of apoplexy, 
or uremia, or dilatation of the heart due to the myocarditis or to an in- 
tercurrent acute pericarditis. 

Irregular Gout. Lithemic or Uric Acid Diatheses. — Gouty Di- 
athesis. — ^Under this title are grouped a great number of minor disturb- 
ances of one or another tissue or organ of the body believed to be due to 
the same defective nitrogenous metabolism which underlies gout. These 
disturbances may affect any part of the body, the eye, the throat, the 



282 



CONSTITUTIONAL DISEASES 



heart, lungs, kidneys, skin, etc. They are met with (1) in persons who 
sulfer from typical gout; (2) in individual members of gouty families, 
who are free from other evidences of the disease; (3) in certain people 
who have never had gout and do not belong to gouty families, but who 
have indulged excessively in food and drink. The evidence of the 
relationship in these latter cases depends wholly upon the curative 
influence of treatment along the lines of gout, and not upon the chance 
finding of uric acid cr^^stals or urates in the urine. There is no question 
that the terms gouty or uric acid diathesis have been used for years 
very loosely to cover many indefinite affections whose only claim to the 
designation lay in the fact that the physician knew no other titles to 
give them and sought support for his diagnosis in the demonstration 
of deposits of uric acid or urates in the urine. On the other hand, there 
is no doubt that the defect in nitrogenous metabolism characteristic of 
gout is capable of producing a great variety of disturbances in different 
parts of the body. The more common are found in (1) the skin. Attacks 
of eczema, psoriasis, or herpes zoster are met with. Eczema of the face, 
ears, or neck is the most frequent. (2) The eye. Conjunctivitis and 
iritis are in some cases of gouty origin. (3) The Throat. — Attacks of 
pharyngitis with much congestion of the tissues are not common. (4) The 
Lungs. — Chronic bronchitis or emphysema, with asthmatic paroxysms, 
may occur. (5) The Heart. — Rapid or irregular action of the heart 
associated with attacks of pain resembling angina pectoris is described. 
(6) The Alimentary Tract. — So-called bilious attacks, marked by con- 
stipation, coating of the tongue, headache, and prostration, may be due 
to this cause. (7) The Urinary Tract. — Renal calculi are common in 
the gouty. Pyelitis, cystitis, or even urethritis may be due to the gouty 
diathesis. (8) The Nervous System. — Headaches, migraine, sciatica, 
neuralgia, cramps in the muscles of the leg and abdomen are found at 
times to be due to a gouty diathesis. 

Retrocedent or Suppressed Gout. — In the course of an acute attack, 
subsidence or improvement in the local conditions may be marked by 
severe internal symptoms, referred especially to the stomach or heart. 
The patient may suffer from abdominal pain, vomiting, diarrhea and 
profound depression and may die in the attack. In other cases the pain 
is referred to the heart and the pulse is rapid or slow and irregular. 
Acute pericarditis sometimes develops under these conditions. 

Urine in Gout. — An immense amount of study has been devoted to 
the urine in gout, , with but small results. A trace of albumin and a 
few hyaline or granular casts are usually found. A trace of sugar is 
not infrequent. In chronic gout the urine shows the evidences of chronic 
interstitial nephritis, is increased in amount, pale and of low specific 
gravity, with a trace of albumin and hyaline or granular casts. The 
excretion of uric acid varies greatly. Before an acute attack for two 
or three days the excretion is diminished. After the attack an increase 
occurs. In chronic gout careful study seems regularly to show a 
diminished excretion. 

Diagnosis. — Typical attacks are easily recognized, but atypical cases 



GOUT 



283 



are often mistaken for rheumatic fever, chronic rheumatism or 
arthritis deformans (see Chronic Polyarthritis). (1) The patient's 
occupation and habits should be noted. In the United States barkeepers 
and brewery men are most often affected. (2) The location of the 
initial arthritis is often suggestive. (3) The presence of tophi in the 
ears, about the joints, or in the subcutaneous tissue is important. They 
must be distinguished from subcutaneous fibrous nodules. (4) The 
attacks of arthritis in gout may be afebrile. (5) Careful study of the 
urine may show a persistent low excretion of uric acid in chronic gout, 
or temporary diminution before an acute attack. No opinion can be 
based on single examinations, and, in fact, the uncertainties still existing 
with relation to the excretion of uric acid in gout render urinary ex- 
aminations of very little service in diagTiosis. 

The BLOOD regularly shows a moderate leukocytosis (15,000-20,000) 
in an acute attack. 

Treatment.— Prophylactic. Abstinence from alcohol, a careful regu- 
lation of the diet so as to avoid an excessive intake of nitrogen, moderate 
exercise in the open air, the free drinking of water, and regular hours 
should be advised for all children of gouty families. 

Of the Acute Attack. — The patient is put to bed and given a milk 
diet. The bowels are opened by a laxative. Colchicum in doses of 20 
minims of the wine or tincture of the seeds is given every two or four 
hours, for the relief of pain. If vomiting or purging is caused, it must 
be stopped. Aspirin, 10 to 20 grains every two hours, may be tried in- 
stead. The affected joint is elevated and wrapped in wool. Lead and 
opium wash or other anodyne applications may be used. After the first 
day or two a purin-free " diet, of eggs, milk, butter, white bread, 
rice, sago, and cheese, may be allowed instead of milk alone. 

Of Chronic Gout.— General.— A carefully regulated life, with diet 
and drink, exercise, bathing, hours of rest defined, is necessary. 

Diet. — Many traditional restrictions and fads are still in vogue, but 
are being swept away by advances in accurate knowledge. Thus red 
meats are no more harmful than any other form of meat. Fruits are 
not objectionable. Vegetable or fruit acids are converted into alkalies 
in the body and are probably beneficial. Mineral waters are no more 
beneficial than any other, some of them may well be harmful. The diet 
must be restricted to the needs of the individual. It is to be general, 
meat being allowed in moderation. Only those foods known to be ex- 
cessively rich in purin bases, such as meat extracts, sweetbreads, liver, 
kidney, or brain, fish roe, caviar, should be prohibited. Among the 
vegetables, cucumbers and tomatoes, and of the fruits, strawberries and 
bananas, are best avoided. The experience of an individual is often 
of more value than the accepted theories. If trial shows that any one 
article of diet brings on joint pains or distress it should be given up ; 
if it can be taken without hnrm, it should bo nllowed. 

Drink. — Coffee, tea, and cocoa have lon^- l)een forbidden because 
believed to contain purin ])ases in excess, but it is not proven that 



284 



CONSTITUTIONAL DISEASES 



caffeine or theobromine can be converted into uric acid and they may 
be allowed in moderation. Water should be drunk freely, particularly 
on rising and before meals. Any pure water can be recommended. No 
advantage has been proven to belong to any of the many mineral waters 
extolled as cures for gout. The mineral content of the water, whether 
of litliia or other salts, is of little moment. Alkalies as such are not of 
special value and alkaline mineral waters are not necessary. Exercise 
should be required, 'but never carried to the point of exhaustion. Walk- 
ing, riding, and golf are especially suitable. 

Hydrotherapy. — Not only the free drinking of water practiced at 
many springs, but the therapeutic application of water in baths, sprays, 
or douches is often very helpful. In the United States the Saratoga, 
Bedford, and White Sulphur Springs are recommended. 

DIABETES MELLITUS 

Definition. — A nutritional disorder characterized by a continued ex- 
cess of sugar in the blood and its excretion in the urine, and by thirst 
and polyuria. The excreted sugar is grape-sugar. 

Etiology. — The disease is relatively infrequent. In the United 
States in 1900 9.3 deaths per 100,000 of population were assigned to this 
cause. (1) Heredity plays a small part in its production, certain 
families showing a predisposition to the disease. (2) It occurs at all 
ages, but children are rarely affected, and its greatest incidence is in the 
decade from 50 to 60 years. (3) Men are affected more often than 
women, in the proportion of 4 to 3. (4) Fright, nervous excitement, or 
over-strain precede the onset in some cases. For this reason men of 
affairs, bank presidents and the like are often subject to this disorder. 
(5) Obesity is a frequent accompaniment, but Von Noorden regards 
it rather as a symptom of the underlying defect in metabolism than as 
a cause. (6) It may follow some of the acute infectious diseases, such 
as typhoid or scarlet fever, diphtheria, or rheumatic fever. (7) Organic 
lesions of the brain, such as tumors, general paresis, cerebral hemorrhage, 
may be followed by diabetes. 

Morbid Anatomy. — The body of a diabetic patient is usually 
markedly emaciated, the skin coarse and dry. Boils or subcutaneous 
abscesses may be present. Not infrequently gangrene of a toe or foot 
is seen. The lungs are frequently the seat of tuberculosis, usually as a 
tuberculous bronchopneumonia. Acute lobar or bronchopneumonia may 
be found. The heart is hypertrophied and arteriosclerosis is marked. 
The liver may be cirrhotic and in rare cases cin'hosis of the liver is 
associated with pigmentation of the skin, the condition described by the 
French as cirrhose pigmentaire diabetique, by others as hemochromatosis. 
The pancreas shows lesions of some kind in about 50 per cent, of the 
cases. Chronic interstitial inflammation with atrophy and hardening 
of the gland is most common. Cysts, tumors, or calculi are found in 
other cases. Microscopically the pancreas shows interstitial inflamma- 



DIABETES MELLITUS 



285 



tion with hyaline degeneration and atrophy, or complete disappearance 
of the islands of Langerhans. The latter is regarded as the essential 
lesion by Opie and other investigators. The kidneys are enlarged and 
show degeneration. Chronic nephritis may occur. The brain and 
nervous system frequently show lesions of varying character. Tumors 
are most frequent; cerebral hemorrhage, and degenerations of chronic 
type are also met with. The blood of the diabetic regularly shows a 
hyperglycemia. 

Metabolism in Diabetes. — The disturbances of metabolism in 
diabetes affect mainly the carbohydrates. Of these three classes are 
distinguished: 1. Monosaccharides or gly coses {CqR-^^^^q) including 
grape-sugar (glucose) or dextrose, fruit-sugar (levulose), galactose and 
mannose. 2. Disaccharides or saccharoses (C'i2H2oOii) including cane- 
sugar (saccharose), milk-sugar (lactose), and maltose. 3. Polysaccharides 
or amyloses (CeH^oOj) including starch, glycogen, and dextrin. The 
carbohydrates, starch, cane-sugar, etc., taken in as food undergo a 
process of digestion and under the influence of the saliva, pancreatic 
juice, and succus entericus are converted into dextrose, which passing 
to the liver is converted by the liver cells into glycogen and there stored 
as such. Glycogen is in turn reconverted into glucose under the action 
of a liver ferment and so supplied to the blood. Glycogen and glucose 
are not derived from carbohydrates alone. A small amount of both can 
be formed from ingested proteid or the proteids of the body. Normally 
the blood contains from .1 to .2 per cent, of glucose. In diabetes there 
is always an excess, a hyperglycemia, amounting in some cases to as 
much as .6 or even .7 per cent. One cause of this hyperglycemia is that 
the liver has lost to some extent its power of storing up as glycogen 
the dextrose supplied to it by the food or the proteids of the body. A 
second element in the production of the hyperglycemia is that certain 
tissues of the body, especially the muscles, have lost, to some extent at 
least, their power of oxidizing the glucose of the blood and converting 
it into water and carbon dioxide. Evidence has been supplied that this 
loss of oxidizing power in the muscles is not due to defect in the muscles 
themselves, but to the absence of a certain glycolytic substance (possibly 
a ferment) normally supplied by the pancreas. 

The glycogenic function of the liver is undoubtedly subject to the 
control of the central nervous system, as is shown by the glycosuria 
which follows experimental puncture of the floor of the fourth ventricle 
in dogs. This nervous control of the glycogenic function of the liver 
would explain the relationship between nervous diseases and diabetes. 
On the other hand, the function of the pancreas in supplying a ferment 
or glycolytic substance which aids the muscles in the assimilation of 
glucose explains the frequency with which pancreatic lesions are found 
to be associated with diabetes, and the glycosuria resulting from the 
experimental removal of the pancreas. 

It would thus appear that diabetes may result from a variety of 
conditions and that no one lesion will exphiin all cases of the disease. 



286 



CONSTITUTIONAL DISEASES 



Symptoms. — The invasion of the disease is insidious. (1) Loss of 
weight associated with languor and weakness usually first attracts atten- 
tion. Some patients, especially the obese, may not lose weight at all, 
but as a rule the loss is steady and progressive. (2) Thirst is more 
active than usual and may be insatiable. (3) The appetite is similarly 
exaggerated and may be enormous. Some patients suffer from gastric 
distress, eructations, and constipation, but in most cases the digestion 




Fig. 59. — A, diabetic gangrene of the great toe; B, diabetic gangrene of the great toe. 



is excellent. (4) Polyuria is marked. In moderate cases three or four 
quarts may be voided, while the output amounts to as much as 5 to 10 
quarts in the severer forms of the disease. (5) The skin becomes dry 
and harsh, the mouth parched, the tongue red and glazed. (6) The 
presence of sugar in the urine is the essential symptom. The urine is 
pale, clear, of specific gravity varying from 1024 to 1045, and usually 
free from all)niiiin or casts. With nephritis albumin and casts appear. 



DIABETES MELLITUS 



287 



Sugar is present in varying amounts, averaging 2 or 3 per cent. In 
severe cases it may amount to 8 or even 10 per cent. The total output 
of sugar in 24 hours varies from a few grains to 1000 or even 1500 
grains. Sugar is demonstrated by Fehling's test and estimated quan- 
titatively by the same test, b}^ fermentation, or the polariscope. The 
fermentation test should always be used to confirm the presence of sugar 
in the urine, for there are a number of other substances which reduce 
Fehling's solution, such as glycuronic acid, homogentisic acid, uric acid 
in excess, lactose, and kreatinin. Acetone, diacetic acid, and fS-oxy- 
butyric acid may also be found in the urine, especially in severe cases, 
by appropriate tests. 

These are the common symptoms of the disease; various others may 
be due to involvement of special organs or to complications of the dis- 
ease. (1) The Skin. — Boils or carbuncles are common and in the im- 
paired state of the diabetic may become grave complications. Eczema 
which may be very annoying may be produced on the genitals, especially 
of women, by the irritation of the urine. Gangrene of the foot or other 
part may occur (see Fig. 59). (2) Respiratory System. — The breath 
often has a sweetish odor, resembling that of acetone. Acute tubercu- 
losis, lobar or bronchopneumonia or gangrene of the lung may develop. 
(3) Circulatory System. — The arteriosclerosis may be the cause of 
symptoms. It underlies the gangrene of the extremities so often seen, 
and may give rise to symptoms of nephritis or myocarditis, or cause 
cerebral hemorrhage. (4) Nervous System. — Headaches may be a 
marked symptom. Neuralgia or neuritis frequently adds to the patient 's 
distress. Sexual power is usually lost. Perforating ulcer of the foot 
is not rare. Degeneration of the posterior columns of the cord present- 
ing symptoms resembling tabes occurs at times. (5) Cataract is not 
uncommon in the elderly patients. Retinitis, atrophy of the optic nerve, 
or paralysis of accommodation may develop. (6) Diabetic coma is the 
most serious complication, being regularly fatal. The type of coma 
varies, (a) Coma with dyspnea, Kussmaul's air-hunger type, is most 
frequent, (b) An alcoholic type with symptoms resembling intoxica- 
tion, (c) Coma with collapse, in which the pulse becomes rapid and 
feeble, the surface livid, the extremities cold. The approach of coma 
may be indicated by lassitude, headache, or restlessness and excitement. 
Drowsiness develops and deepens into coma, from which, as a rule, the 
patient never rouses. Diabetic coma has been proven to be the result 
of the acid intoxication caused by the ^-oxybutyric acid, and its presence 
in any considerable amount is always a warning of the approach of 
coma. When /?-oxybutyric acid is present, acetone and diacetic acid are 
also found, and because of the difficulty surrounding the tests for 
j8-oxybutyric acid, acetone and diacetic acid are first tested for. If 
present, ^-oxybutyric acid must be tested for, but if there is no acetone 
or diacetic acid, we may conclude that ^-oxybiityric is not present. 

Course and Prognosis. — In children dial)('t('s is usually swiftly 
fatal. Adults also sometimes succumb quickly, but as a rule the course 



288 



CONSTITUTIONAL DISEASES 



of the disease is protracted over several years. The older the patient 
the less effect diabetes seems to have. Obese people also seem to bear 
the disease well. 

Diagnosis. — This depends chiefly on the examination of the urine. 
The sugar must be shown to be persistently present, and proven to 
be grape-sugar, to justify the diagnosis. Temporary glycosuria from 
any of the following causes must be excluded: (a) narcosis from ether, 
alcohol, or opium, or coma from any cause; (b) carbon dioxide, amyl 
nitrite, mercury, or strychnine poisoning; (c) epilepsy, hysteria, or 
neurasthenia; (d) chlorosis or exophthalmic goitre ; (e) acute infectious 
diseases. If the characteristic symptoms of diabetes be absent some 
days of observation may be required to determine the question. The 
possibility of deception by the addition of sugar to normal urine must 
be considered in some cases. 

Treatment. — Hygienic. — A carefully regulated life, free from worry 
or care, is necessary. Daily lukewarm baths serve to prevent some 
of the skin complications. Moderate exercise, if the patient's condition 
permits it, is desirable. Constipation must be corrected. Dietetic. — 
The hope of cure in diabetes lies in the proper management of the diet. 
The principle upon which the diet is managed is that if the patient can 
take even the smallest amount of carbohydrate food without excreting 
sugar, the tolerance of carbohydrates can be raised gradually, the amount 
of carbohydrates well-borne can be increased and ultimate cure may be 
brought about. In the beginning the amount of sugar excreted, while 
the patient takes an ordinarv^ mixed diet, should be determined for 
several successive days. The urine should also be tested by fermentation 
to confirm the findings of other tests. The patient should then be put 
upon a diet free of starches and sugar, such as the following: 

Breakfast: 7.30 a.m. 120 grams beefsteak or mutton chops, two 
boiled or poached eggs, 200 c.c. coffee or tea without sugar. 

Lunch: 12.30 p.m. 200 grams cold roast beef, mutton, or chicken; 
60 grams of celery, cucumbers or tomatoes with 5 c.c. vinegar, 10 c.c. of 
oil, pepper and salt as required; 20 c.c. whiskey; 400 c.c. water; 60 
c.c. coffee. 

Dinner: 6 p.m. 200 c.c. clear bouillon; 200 grams roast beef; 60 
grams lettuce with 10 c.c. vinegar, 20 c.c. of olive oil or ahree table- 
spoonfuls of some green vegetable, such as spinach; 20 c.c. whiskey 
(if desired) ; 400 c.c. ApoUinaris or Avater. 

Supper: 9 p.m. 2 eggs raw or cooked; 400 c.c. ApoUinaris or water. 

About 15 grams of butter may be given daily npon the eggs or in 
gravies. Saccharin may be substituted for sugar. No milk or cream 
is to be allowed. 

If the examination of 24-hour specimens of urine shows no sugar for 
several days, the disease is of mild type and starches may be added, 
80 grams of bread being alloAved the first day and the amount later 
increased if no sugar appears. Later potatoes and other vegetables 
may be added. If sugar continues to appear in the urine on the re- 



DIABETES INSIPIDUS 



289 



stricted diet, Naunyn advises a fast-day. If the amount of sugar is 
small this will sometimes cause it to disappear altogether, and tolerance 
for minute amounts of carbohydrates may then be tried. If persistent 
trials fail to free the urine of sugar, carbohydrate food must be allowed 
in moderate amounts, as these patients do badly if restricted too long 
to the proteid diet, and the danger of coma is increased. In these cases 
trial must be made to find just what amount of carbohydrates must be 
allowed to maintain strength and nutrition and not too greatly increase 
the amount of sugar in the urine. 

A great variety of medicines have been given in diabetes, but none 
has any definite effect upon the process. Opium and codeine have been 
especially used. They serve to lessen distress or pain, but they increase 
the tendency to constipation, and their administration should be avoided, 
unless required for the relief of suffering. Pancreatic extracts have 
been given, but without success. Arsenic in the form of Fowler's 
solution, or as arsenious acid, has been much praised. Sodium bromide, 
phenacetin, the salicylates and many other drugs have been employed 
at various times, but no confidence can be placed in their effects. 

Treatment of Diabetic Coma. — The presence of /5-oxybutyric or 
diacetic acids in the urine must always be regarded with concern, 
although occasionally a patient's urine shows their presence for many 
weeks without harmful results. In moderate cases, when these acids 
appear, effort should be made to reduce them by increasing the amount 
of carbohydrate food, especially if the intake of starches and sugars has 
been much restricted. A moderate increase in the allowance may cause 
the disappearance of the acids. Since it has been shown that the harmful 
acids are derived not from the carbohydrates, but the fats, the latter 
should be materially reduced or excluded from the diet. Subcutaneous 
injections of levulose in 5 to 10 per cent, solutions have recently been 
recommended by Von Noorden. Others give levulose by mouth. Sodium 
carbonate or bicarbonate must also be given by mouth, rectum or sub- 
cutaneously, in very large amounts. From 1 to 2 drams hourly by 
mouth, and twice as much by rectum may be given. For intravenous 
injection a 3 to 5 per cent, solution, carefully sterilized, is used. From 
1 to 2.5 ounces of sodium bicarbonate have been given at one injection. 
Threatened coma may be temporarily relieved by these measures, but 
the fatal outcome cannot be long delayed. 

Pruritus is best treated by reducing the amount of sugar in the urine. 
Lotions of boric acid or hyposulphite of soda (30 grains to the quart) 
may give temporary relief. Boils, carbuncles, or gangrene must be 
treated aseptically. Operations are likely to induce coma, but the 
danger of septic infection is great. 

DIABETES INSIPIDUS 
Definition. — A rare disorder characterized by the persistent passage 
of large quantities of urine free from sugar, albumin, or casts. 

Etiology. — ^Young people are most often affected. 1. Various affec- 
19 



290^ CONSTITUTIONAL DISEASES 



tions (a) Trauma or tumors of the brain, especially those involving' the 
• floor of the fourth ventricle, may be the cause, (b) Cerebral syphilis has 
preceded some cases. (c) Hysteria, epilepsy, or neurasthenia may 
accompany the polyuria. 2. The disease may be idiopathic, no cause 
being ascertainable. The majority of cases belong in this group. 

Morbid Anatomy. — No constant pathological changes are found. 
The brain lesions mentioned above may be present. The kidneys and 
bladder are sometimes enlarged. 

Symptoms. — Polyuria is the essential symptom. Enormous quan- 
tities of urine are passed, amounting in some cases to 15 or 16 quarts. 
The urine is consequently water-like, its specific gravity 1001-1005, 
almost colorless. It contains no sugar, no albumin or casts, as a rule, 
although traces of albumin may at times appear. Increased thirst and 
appetite are commonly associated. Nutrition is usually unimpaired, but 
sometimes suffers severely. The temperature is subnormal. The course 
of the disease is usually very chronic, the patients ultimately become 
exhausted and die in coma. 

Diagnosis. — Diabetes mellitus is excluded by the examination of 
the urine; chronic interstitial nephritis by the urinary conditions and 
the absence of arteriosclerosis and h3^pertrophy of the heart. A dis- 
tinction cannot always be drawn between a symptomatic polyuria and 
diabetes insipidus. In fact, some writers exclude the polyuria of hysteria 
or epilepsy from the disease, others include it. If the condition is per- 
sistent it may be termed diabetes insipidus. 

Treatment. — Codeine or opium may be given to lessen thirst and 
thus reduce the polyuria. Valerian is more often prescribed, in 5 
grain doses of the powder or 15 grains of the valerianate of zinc three 
times a day. The doses may be gradually increased. If cerebral 
syphilis is suspected specific treatment is in order. 

RACHITIS 
(Rickets) 

Definition. — A disease of infancy and childhood caused by defective 
nutrition, with its most striking manifestations in the growing bones. 

Etiology. — The disease regularly develops between the ages of 3 
months and 3 years. Both sexes are affected. AVhile it is much more 
common among the children of the poor in large cities, it is frequently 
met with in country children and in those of wealthy parents. What- 
ever influences lower the vitality of children, such as illness of the 
mother during pregnancy or lactation, poverty, overcrowding, lack of 
sunlight, acute disease, especially of the digestive organs, predispose to 
the development of rickets. The essential cause, however, is defective 
nutrition. This may be brought about either by improper feeding or by 
defective assimilation of proper food because of inherent weakness of 
digestion and assimilation, (a) Improper feeding is by all odds the 
most common cause. Nursing children very rarely develop rickets. 
Artificially-fed children frequently do so. Artificial foods containing 



KACHITIS 



291 



an excess of carbohydrate materials, condensed milk, or cow's milk too 
greatly diluted, are the foods upon which rickets is most often developed, 
(b) Defective digestion or defective assimilation is apparently the 
cause of rickets in some children who have been most carefully fed. 
Such defective digestion is most often due either to inherent feebleness 
of the child or to intercurrent diseases of the alimentary tract, such as 
ileocolitis. 

Morbid Anatomy. — The most striking changes are in the bony 
skeleton. The head is large, the frontal bosses prominent and the skull 
at these points thick. Craniotabes is often present in the occipital 
regions where the bones are subjected to pressure. The maxillae are 
usually small and imperfectly developed. The teeth are late in appear- 
ing. The thorax often shows lateral grooves along the line of attach- 
ment of the diaphragm with flaring of the free borders of the ribs below. 
The junctions of the ribs and cartilages are regularly enlarged, forming 
the so-called rachitic rosary. The abdomen is prominent; the muscles, 
both of trunk and extremities, flabby. The long bones are frequently 
deformed, the lower extremities showing bow-legs or knock-knee, the 
upper, abnormal curv^ature of the humerus, radius and ulna. The clavicle 
is often unduly curved. The spine is markedly curved and may appear 
kyphotic. The junctions of epiphysis and diaphysis of the long bones, 
especially at the wist, ankle, and knee, are regularly enlarged. Bron- 
chitis or bronchopneumonia is almost invariably present post-mortem. 
The liver and spleen are sometimes enlarged. The characteristic lesion 
of rickets i& found in the costo-chondral junctions or the junction of 
epiphysis and diaphysis of the long bones. In rickets this junction is 
enlarged both laterally and longitudinally, and instead of the normal 
sharp line of demarcation between the two the line is wavy and indis- 
tinct. These changes are visible to the naked eye. Microscopically the 
zone between epiphysis and diaphysis is found unduly vascular and with 
a very irregular distribution of cartilage cells and islets of calcification. 
The cancellous tissue of the shaft is also unduly vascular and ossification 
is imperfect, so that the bones are soft and easily deformed. The sub- 
periosteal bone formation shows a similar vascularity and imperfect 
ossification, so that some areas (frontal bosses) are thickened, and others 
unduly thin (occipital bones) . 

Symptoms. — General. — While the skeletal signs of rickets are 
always the more impressive symptoms, the constitutional effects of the 
disease are the more important. Head-sweating and restless tossing of 
the head are common, so that the hair over the occiput is worn thin by 
friction. IMouth-breathing due to adenoids is common, and the lymphatic 
nodes dre generally enlarged. The rachitic child suffers from frequent 
attacks of bronchitis or bronchopneumonia. The digestion is impaired, 
with flatulence and constipation usually present. In some cases ileo- 
colitis with diarrhea develops. The general nutrition suffers little and 
rachitic children often appear well-nourished or fat, but the tissues, 
especially the muscles, are flabby. The children are consequently late 



292 



CONSTITUTIONAL DISEASES 



in walking. The teeth are late in appearing. Resistance to infection is 
lowered and rachitic children succumb easily to acute infectious diseases, 
especially to measles or diphtheria. 

Skeletal. — These have been described under the morbid anatomy. 
The open fontanel, prominent frontal bosses, small jaw-bones, the curv- 
atures of the long bones, the rachitic rosary are all seen in marked cases. 
In the milder cases only the beading of the ribs, the delayed dentition, 
or open fontanel indicates the presence of the disease. Pelvic deformities 
not of importance during childhood, but of gravest moment in adult 
women, are common. Owing to contraction of the pelvis, enlargement 
of liver and spleen and distention of the intestines by gas, the abdomen 
is regularly prominent and tympanitic. 




Fig. 60. — Achondroplasia. Note the large head, the comparatively normal body, the shortness 
of the extremities, particularly the upper arms and thighs, and the deformities. From the collection 
of Dr. W. P. Northrup. 

Course and Prognosis. — Rickets, rarely fatal in itself, leads to high 
mortality through death from complicating bronchitis or broncho- 
pneumonia or acute infectious disease. Those who survive the disease 
recover slowly with more or less permanent deformity of the skeleton. 
The great majority of cases of knock-knee and bow-legs are due to 
rickets. 

Diagnosis. — The rachitic rosary, delayed dentition, open fontanel, 
and enlarged epiphyses, without the advanced skeletal changes, make the 
diagnosis easy if these signs are looked for. 

Treatment. — Hygienic. — Fresh air and sunlight are of great value. 
Systematic bathing, a bath of 85°, followed by sponging mth slightly 
cooler water, should be practiced. Massage may be given. The child 
must be kept off the feet until the bones have become strong enough to 
bear the weight. 



ACHONDROPLASIA 



293 



Dietetic. — Change of food is the essential measure. Carbohydrates, 
if in excess, must be reduced and fat given. Breast milk is ideal for 
the young. In older children a proper dilution of cow's milk in which 
the percentage of fat is steadily increased is given. Cod-liver oil may 
also be prescribed, most easily in a malt extract. Phosphorus is highly 
commended, 6 to 15 drops of the elixir (U. S. P.) three times a day. 

ACHONDROPLASIA 

Definition. — A developmental disease which impairs the cartilaginous 
ossification, especially in the long bones. 

Etiology. — Heredity plays an important role. The disease has re- 
peatedly been observed in successive generations. Several members of 
one family may likewise be affected, especially in the case of very large 
families. 

Of the nature of the disease little is known. It presents certain 
resemblances to rickets, syphilis, and cretinism, which have been regarded 
as indicating relationship by various w^riters, but our knowledge of the 
disease at present leads to its classification as a separate clinical entity, 
but does not enable us to exactly determine these questions. 

Morbid Anatomy. — The lesions are found in the bones, especially 
the long bones. The extremities are short, the shortening affecting 
chiefly the proximal segments, arm and thigh. The trunk is practically 
normal, although there may be a moderate enlargement of the costo- 
chondral functions reproducing the rachitic rosary. The head is large 
with prominent bosses. Premature synostosis of the bones surrounding 
the foramen magnum and likewise of the junction of the occipital and 
sphenoid bones is found. The vertebrae are normal. 

Microscopic examination shows the fundamental error to be defec- 
tive cartilage formation. Thus the rosary is not due, as in rickets, to 
swelling of the cartilage, but to defective development of cartilage 
with excessive formation of bone in the rib-end, so that the cartilage 
may lie in a bony cap. 

The cartilage is abnormal throughout, thinner than it should be, 
more fibrous, sometimes vacuolated, with an absence of the normal zone 
of proliferation, hence the name achondroplasia. 

In some instances the epiphyses are almost entirely absent, and the 
shortness of the long bones is readily explained. 

Symptoms. — Most achondroplasiacs are still-born and the disease is 
best known from the studios of such skeletons. Those that survive con- 
stitute one of the well-recognized types of dwarfs. The essential features 
are the large head with prominent bosses, the almost normal trunk, with 
the disproportionately short extremities, the shortening affecting espe- 
cially the arm (humerus) and thigh (femur). Deformities of the ex- 
tremities, especially knock-knee, are common (see Fig. 60). The hands 
are small, short, and cubical, the fingers being all of nearly the same 
length. The fingers often diverge like the prongs of a trident. 



294 



CONSTITUTIONAL DISEASES 



Teething, talldng, and walking are not delayed as in rickets, and the 
mentality of most of these dwarfs is normal. Some of them are unusually 
bright. 

Diagnosis. — This must be based in the living upon the skeletal 
characters above noted. The affection must be distinguished from the 
others forms of dwarfism, especially infantilism, cretinism, and rickets. 

Infantilism is marked by the failure of growth with preservation 
of the normal relations in length and size of parts, and absence of the 
secondary sexual characteristics. Achondroplasiacs have the skeletal ab- 
normalities, but develop sexually. 

Eickets is distinguished by the abnormally large epiphyses, the 
deformed extremities, which are, however, of normal relations as to 
length, the wide-open fontanel, the delay in teething, walking and 
talking. 

Cretins are easily distinguished by the characteristics noted on page 
272. 

Treatment. — No treatment is known to have any influence upon the 
disease, but careful feeding, massage, passive movements, and electricity 
are indicated. 

OBESITY 

Definition. — A metabolic disorder characterized by the deposition 
of excessive amounts of fat. 

Etiology. — (1) Heredity plays an important role. The tendency to 
obesity is transmitted in certain families, especially in those subject to 
gout. (2) The disorder sometimes dates from birth, but usually ap- 
pears between the ages of 30 and 50 years. (3) Women are more often 
affected than men. In women repeated pregnancies seem to favor obesity 
and the increase in weight frequently dates from child-birth or mis- 
carriage. (4) Persons who lead a quiet, sedentary life are most subject 
to the disorder. (5) The prime factor is the habitual ingestion of 
excessive amounts of food^ especially carbohydrates and fats, and often 
also the use of malt liquors, or sweet wines. 

Metabolism in Obesity. — The essential feature of obesity is the 
ingestion of more food than can be oxidized and turned into energy. 
Carbohydrates and fat most readily yield fat, but fat can also be formed 
from proteid foods. The problem of obesity is for the most part a purely 
mathematical one between the energy required by the body and that 
supplied by the food. A peculiar tendency to the formation of fat, 
based upon disordered metabolism, is claimed to exist in certain 
individuals, so that they increase their fat while living very abstemiously. 
While this has never been thoroughly proven, it is generally accepted 
that such a disorder of metabolism, essentially a diminished power of 
oxidation, does exist. Anemia lessens the oxidation power and is not an 
infrequent accompaniment of obesity. 

Morbid Anatomy. — Fat is found especially in the subcutaneous 
tissues, particulai'ly those of the abdomen, in the omentum and mesen- 



OBESITY 



295 



tery, about the heart and kidneys, and in the liver. The heart is 
enlarged, the right side dilated, and much fat is found on the surface 
and also infiltrating the heart muscle. The liver is very fatty. 

Symptoms. — Obesity is consistent in some cases with perfect health 
and great activity. In most instances the increasing weight leads to 
diminished activity, because every effort demands greater exertion, and 
the subjects become inactive both mentally and physically, and this 
inactivity still further increases the tendency to obesity. Obesity is 
regularly accompanied by diminished power of resistance to disease or 
shock, and very fat persons are poor subjects for acute infections, such 
as typhoid fever or pneumonia, or surgical operations. In some cases 
the fatty infiltration of the heart produces symptoms of feebleness and 
irregularity of the heart action (see Fatty Heart). 

Treatment. — Alcohol must be forbidden and the total amount of 
food and drink reduced. Banting reduced the total diet to from 21 to 
27 ounces, of which 13 to 16 were of animal food, and only 2 of bread. 
Sugar and other starches were excluded. Ebstein would allow fats 
because they produce satiety. Ebstein 's dietary is as follows : 

Breakfast: Toasted white bread, 2 ounces. Tea without milk or 
sugar, 8 to 9 ounces. 

Dinner: Soup made with beef marrow. Fat meat, 4 to 5 ounces, 
and a moderate allowance of spinach, beans, peas, cabbage, or asparagus. 
Light white wine, 2 or 3 glasses. Tea, as before. 

Supper: An egg, a little roast meat, with fat. Bread, 1 ounce, 
with butter. Tea, as before. 

Oertel's diet would allow less fat and more proteid, and is ordered 
as follows : 

Morning: Coffee or tea with milk, 6 ounces. Bread, 3 ounces. 

Noon : Soup, 4 ounces. Roast beef or other meat, 7 to 8 ounces ; 
salad or light vegetable ; a little fish ; bread or other farinaceous pud- 
ding, 1 ounce; fruit, 3 to 6 ounces. 

No liquids except in hot weather, 6 ounces of light wine. 

Afternoon: Coffee or tea, 6 ounces. Occasionally bread, 1 ounce. 

Evening : Eggs, 1 or 2 ; bread, 1 ounce ; perhaps a small bit of 
cheese, a little salad, and fruit; light wine, 6 to 8 ounces, with 4 or 5 
ounces of water. The amount of water is restricted to 1 pint. 

Such a dietary is regularly combined Avith progressive exercise, the 
patient being required to walk carefully graduated distances, involving 
increasing effort, either on the level or on hills. Hot baths, even the 
Turkish bath, may be employed in certain cases. 



VII 



INTOXICATIONS AND MISCELLANEOUS 
DISEASES 

ALCOHOLISM 

INEBRIETY OR DRUNKENNESS 

Definition. — An acute or chronic intoxication due to the excessive 
use of alcoholic drinks. 

Etiology. — (1) Heredity plays an important role, probably through 
the transmission of an inherently weak and unstable nervous system. 
(2) This inherent weakness of the nervous system is the basis of 
excessive indulgence in most cases, and for this reason alcoholism, both 
acute and chronic, is now looked upon as a disease rather than a 
habit. (3) ]\Iany other factors enter into the causation of alcoholism in 
individual cases, such as the force of example, social custom, the fatigue 
of exhausting labor, a false belief that the use of alcohol gives strength, 
and the like. Occupations involving the handling of liquors are 
especially perilous. 

Symptoms. — (1) Acute Alcoholism. — The ingestion of alcohol 
causes a primary stimulation, soon followed by marked fatigue and 
exhaustion, affecting chiefly the circulatory and nervous systems. The 
face flushes and the pulse becomes rapid and bounding. Stimulation 
of the cerebral cortex is shown by unusual animation and the rapid 
flow of ideas. Peculiarities of disposition are accentuated and the 
individual becomes more affectionate or quarrelsome. jMuscular inco- 
ordination soon develops, the victim staggers and loses control of his 
movements. The mind becomes dulled, stupor, and finally coma super- 
vene. In this state the face is flushed, the pupils dilated, normal, or 
contracted, but not unequal; the pulse rapid, full and bounding; and 
the breath smells strongly of alcohol. IMuscular twitchings are not 
uncommon, and general convulsions may occur in certain persons. The 
alcoholic coma is rarely profound ; the patient can be roused by slapping 
the face, or steady pressure over the supra-orbital nerves, and will then 
move all his extremities, struggling and using abusive language. In 
alcoholic coma the temperature is often subnormal, sometimes below 95°. 

Diagnosis. — Difficulty in the recognition of acute alcoholism is rare. 
Two sources of error should be avoided: (1) Persons suffering from 
other severe affections may be given sufficient alcohol to taint the 
breath. (2) Drunken persons by falling or being struck frequently 
suffer severe injuries, such as fracture of the skull, the symptoms of 
which may be concealed by the intoxication. (For the differential 
diagnosis of alcoholic coma see ITremia.) Grave errors are frequently 
made by ambulance or police surgeons in large cities. To avoid these 
the only safeguard lies in having everv^ comatose x')atient cared for and 
observed carefully until the diagnosis is established beyond doubt, or 
he has fully roused from the coma. 
29fi 



ALCOHOLISM 



297 



Treatment. — The stomach, should be thoroughly emptied, by washing 
if feasible. The patient may then be allowed to sleep off the stupor. 
A dose or two of aromatic spirits of ammonia, one-half to one dram, 
often aids in recovery. In severe cases with subnormal temperature 
external heat and cardiac stimulants (caffeine or strychnine) may be 
necessary. 

(2) Chronic Alcoholism. — Constant or periodic excess in the end 
leads to the condition denominated chronic alcoholism. The habitual 
use of alcohol is a common cause of chronic gastritis, cirrhosis of the 
liver, chronic nephritis, arteriosclerosis, and polyneuritis, and many 
cases of chronic alcoholism present one or more of these conditions. 
The more characteristic symptoms are referable to the influence of alcohol 
upon the nervous system. In the brain, cord, and peripheral nerves 
chronic inflammatory and degenerative changes are demonstrable. The 
distribution of the lesions and the symptoms resulting therefrom vary 
in different cases and several clinical affections have been described. 

Symptoms. — Many persons use alcoholic beverages in excess for 
years without serious symptoms. Others show tremors of the hand and 
tongue, increasing mental dulness and apathy, forgetfulness, irritability 
of temper, disregard of duty and all moral obligations, and finally 
complete moral and physical degeneration. The facies of the chronic 
alcoholic patient is often characteristic. The eyes are watery, the 
conjunctivae congested, the nose and cheeks deep red with prominent 
dilated veins, the expression dull and the speech slow and imperfect. 
Various forms of insanity, especially dementia paralytica, may end 
the course. 

Treatment. — Control, moral and possibly physical, is of prime im- 
portance. Institutional treatment is therefore often necessary. The 
organic lesions of the patient, gastritis, nephritis, etc., must be ap- 
propriately treated, and every effort made to restore bodily vigor by 
diet and exercise. For the habit itself the hypodermic administration 
of atropine and strychnine, gr. 1/100 each, three times a day, with 
gradual reduction of the dose, has been found useful. The Towns-Lam- 
bert method of treating drug habits may be employed. 

In treating an alcoholic the purgatives (see p. 300) and the initial 
dose of the belladonna mixture are given at the same time. The bella- 
donna mixture is continued day and night. At the 12th, 24th, and 36th 
hours the cathartics are repeated. After the appearance of charac- 
teristic bilious green stools, the castor oil is given, about the 44th or 
45th hour. 

Occasionally the treatment is continued over an additional period, 
the cathartics being given at the 48th hour and the treatment continued 
till 60 hours have elapsed. 

Alcohol is given only to elderly or very nervous patients, who are 
allowed four or five doses of whiskey, 2 ounces each, during the first 
24 hours. Sedatives are often required to produce sleep and cardiac 
stimulants are given after the first 24 hours, or earlier, if necessary. 



298 IxNTOXICATIONS— MISCELLANEOUS DISEASES 



Delirium Tremens. — This affection occurs in the coarse of chronic 
alcoholism (1) following a debauch or (2) after an injury, a surgical 
operation, or acute illness. Deliriiun tremens is frequently seen after 
severe fractures, or operations of any kind, or complicating pneumonia, 
erysipelas, and like acute infections. 

Symptoms. — The attack begins Avith restlessness, insomnia, and 
headache. The tremor of fingers and tongue is marked. The tongue 
is coated and the appetite lost. Soon the characteristic hallucinations 
develop, the patient seeing snakes, rats, mice, and hearing angels or 
demons speaking to him. An active delirium follows in which the 
patient struggles to escape from bed, talking or shouting incessantly, 
grasping or striking at imaginary creatures in the air or upon the bed, 
his eyes expressing wild excitement or fear. Very rarely the delirium 
is of pleasant character. The temperature is raised, the pulse rapid 
and bounding, or later weak and small. The delirium after three or four 
days subsides gradually or the patient succumbs to exhaustion. 

Diagnosis. — The tremor of hands and tongue, and the hallucinations 
are characteristic. Careful physical examination is essential to exclude 
the presence of injury, such as fracture of the ribs or an extremity, 
pneumonia, erysipelas, or other intercurrent disease. 

Treatment. — Restraint is necessary and is best effected by careful 
attendants, otherwise by sheets or straps which confine the arms and 
legs, while not restraining the movements of the body or respiration. 
Rest and food are the essentials. Chloral and bromide of soda are 
given in doses of ten to fifteen grains of the former to twenty or thirty 
of the latter every two or three hours. Paraldehyde in doses of one 
to two drams by mouth or rectum is valuable. Hyoscine liydrobromate, 
gr. 1/100, may be given occasionally. Morphine is rarely satisfactory 
and always dangerous in this condition, too great respiratory^ depression 
being produced by doses sufficient to quiet the patient. IMilk, broths 
and eggs should be given as freely as possible. A continued hot bath is 
advised for the delirium, where circumstances permit sufficient attend- 
ants to carry out the procedure. 

Serous Meningitis or Wet-brain. — Following a debauch or an 
attack of delirium tremens alcoholic patients sometimes develop the so- 
called alcoholic or serous meningitis. More accurately speaking, it is an 
edema of the pia mater. The patient sinks into a stupor, with stiff neck, 
somewhat contracted pupils, hyperesthesia of the skin, and sensitiveness 
to pressure of the extremities, and sometimes rigidity, the temperature 
normal or slightly raised, the pulse rapid and weak. After some days 
the patient improves or the stupor deepens and he succumbs to ex- 
haustion or intercurrent pneumonia. The condition may last three or 
four weeks. 

Treatment. — Careful feeding is important. Strychnine, gr. 1 ^60- 
1/30, and ergot, 30 minims of the fluidextract or its equivalent, should be 
given hypodermatically eYery two hours. Camphor and caffeine may 
also be used. 



MORPHINE OR OPIUM HABIT 



299 



OPIUM POISONING AND MORPHINISM 

Acute Poisoning. — An overdose of opium or morphine produces a 
very characteristic picture of increasing drowsiness ending in coma, 
with pupils contracted to the last degree (pin-point), respiration falling 
to 12, 10, or even 6 a minute, and finally ceasing with death from 
asphyxia. 

Treatment. — The stomach should be washed out with a 1/500 solution 
of potassium permanganate, since morphine even when taken hypo- 
dermatically is excreted in part by the stomach, and the permanganate 
has been shown to prevent the toxic action of opium or morphine. The 
washing is repeated if the poisoning is severe. Atropine, gr. 1/100 or 
more, is given as an antidote, and repeated as indicated. Black coffee 
is given by rectum. Artificial respiration must be kept up for hours, if 
necessary. For this purpose the Fell-O'Dwyer apparatus is invaluable. 

MORPHINE OR OPIUM HABIT 

Definition. — A chronic intoxication with opium or one of its deriva- 
tives, usually morphine. 

Etiology. — (1) A fundamental weakness of the nervous system, as 
in other evil habits, is present in many cases. (2) The influence of 
temptation is seen in the fact that druggists, physicians and nurses are 
so frequently victims of the habit. (3) Painful affections, such as 
neuralgias, dysmenorrhea, endometritis, etc., or insomnia are often the 
explanation of the beginning of the habit. The use of morphine or 
opium for the relief of any distress likely to be persistent is therefore 
attended with great danger. 

Symptoms. — Opium or morphine is occasionally used for some time 
without serious symptoms. Most persons give early evidences of the 
habit. These are first seen in the alternations of the exhilaration produced 
by the taking of the drug and the depression which naturally follows. 
Immediately following the indulgence the habitue is stimulated, the 
eyes are bright, the pupils contracted, the cheeks flushed, the mind 
alert and active, and the appetite increased. Itching of the nose re- 
quiring frequent rubbing is often notable. As this effect wears off the 
individual becomes dull and drowsy, the pupils dilate, the patient is 
morose and irritable, without energy or inclination to exertion of any 
kind. These alternations present themselves more and more frequently, 
requiring larger doses and more frequent administrations to satisfy the 
longing for the drug. Gradually a condition of malnutrition develops, 
the patient loses appetite altogether, suffers from chronic constipation, 
the hair becomes gray, the skin dry and parchment-like, and flesh and 
strength fail. If the drug is taken hypodermatically, abscesses fre- 
quently develop in the various punctures. But the most striking effect 
of the habitual use of opium is, in most cases, the total failure of the 



300 INTOXICATIONS— MISCELLANEOUS DISEASES 



moral nature. The victims become most adept liars, and unable to tell 
the truth. They become oblivious to all ordinary moral impulses, but 
are rarely, like the alcoholic, abusive or destructive. 

Diagnosis. — The alternation in the condition of the patient from 
time to time is suggestive of a drug habit. The contracted pupils and 
itching of the nose point to opium or morphine. The marks of the 
hypodermic needle can often be found. 

Treatment. — Because of the deception practiced by patients and 
their absolute untrustworthiness and inability to tell the truth, the 
treatment of these patients outside of institutions where they can be 
kept under constant supervision and controlled to some extent is regu- 
larly futile. The individual who really desires to escape from his habit 
and will honestly co-operate with his physicians is rare indeed. The 
principles of the treatment in institutions are the gradual withdrawal 
of the drug, the relief of distress and craving by ergot and bromides, 
hot baths or cold packs, and the building up of the patient by careful 
feeding and tonics, especially nux vomica or strychnine. 

The Towns-Lambert method of treatment of drug habits has been 
widely tested and found effective. The essentials of the treatment of 
morphinism consist in the thorough purgation of the patient, followed 
by the administration of fractional parts of the customary daily dose 
of morphine at stated intervals and also of a mixture composed of 15 
per cent, tincture of belladonna, two parts, and one part each of the 
fluidextracts of hyoscyamus and xanthoxylum. The treatment is out- 
lined as follows: At the outset the patient is purged by the adminis- 
tration of five compound cathartic pills and five grains of blue mass, 
followed, if necessary, by a saline after six or eight hours. After three 
or four movements two-thirds of the daily allowance of morphine is 
given in three divided doses ( % each) at one-half -hour intervals. 
Eighteen hours later one-half of this dose is administered, and again 
after eighteen hours one-half of this dose (one-sixth the original dose). 
Ten hours after each dose of morphine the purgation is repeated as at 
the outset^ and finally about the fifty-sixth hour of treatment two ounces 
of castor oil are given. The belladonna mixture is given day and night, 
beginning with doses of six drops hourly, and increasing the dose two 
drops every six hours till sixteen drops are given, the mixture being 
diminished or stopped if symptoms of belladonna poisoning appear. 

Among the symptoms of poisoning noted are dilation of the pupils, 
a dryness of the throat or redness of the skin, a peculiar incisive or 
insistent voice, and insistence on one or two ideas. The mixture is 
renewed at a lower dosage on the subsidence of these symptoms, but is 
continued throughout the treatment. Nervousness and discomfort are 
treated by hypodermic injections of codeine, in doses sometimes as large 
as five grains, repeated as necessary. Stimulants, such as strychnine and 
digitalis, are given about the thirtieth hour of treatment, and after the 
withdrawal of the drug tonics, such as phosphorus and arsenic. Careful 
feeding is necessary in the after-treatment. 



COCAINE POISONING 



301 



COCAINE POISONING 

Acute poisoning is rarely seen except from excessive doses in surgery. 
Nervous excitement, rapidity and weakness of the pulse, with pallor and 
finally collapse, may be produced. The treatment is purely symptomatic, 
by sedatives and stimulants as reciuired. 

COCAINISM OR COCAINE HABIT 

The habitual use of cocaine is increasing. It is rarely taken alone, 
but the subjects often indulge in morphine, alcohol, or other drugs. 

Etiology. — (1) The habit is frequently developed from the use of 
nostrums advertised as catarrh cures and containing cocaine in quantity. 
(2) The drug may be taken for the relief of physical exhaustion or 
pain. (3) In the large cities the taking of cocaine has become one of 
the established modes of debauchery. 

Symptoms. — These are difficult to detect or describe because the 
cocaine is so often used together with other drugs. Alternating periods 
of exhilaration with increased mental and physical activity and de- 
pression with irritability and sluggishness occur, and become more and 
more frequent. The exhilaration usually follows an opportunity to take 
the drug and by being alone. The victims develop the unreliabilit}^ of 
character seen in other drug habits, become slothful, indolent, anemic 
and poorly nourished. Not infrequently the habit results in insanity, 
with hallucinations and delusions. 

Diagnosis. — This is difficult, unless the drug is found in the posses- 
sion of the patient or acknowledged by him. The alternations of 
exhilaration and depression and the changes in character are suggestive 
of drug-taking. The cocaine-taker seeks to be alone and is very secretive 
regarding his habits, in this differing from the alcoholic ; on the other 
hand, the contraction of the pupils and the itching of the nose char- 
acteristic of morphine are not observed. 

Treatment. — This, as in morphine taking, is best done in institutions, 
and for the same reason. The drug is withdrawn gradually and 
sedatives or stimulants administered as required, while everv^ effort is 
made by careful feeding and nursing and hydrotherapy to improve the 
general condition. 

Cocainism may be treated in the same manner as morphinism (see 
p. 300), except that no cocaine is given and cardiac stimulants are 
administered from the beginning. 

CHRONIC LEAD POISONING 

(Plumbism. Saturnism) 

Etiology. — The disease is produced through the taking in of lead 
either by the alimentary or respiratory tracts or by the skin. There 
is no special susceptibility of age, race, or sex, but men are most often 



802 INTOXICATIONS— MISCELLANEOUS DISEASES 



affected by reason of exposure. Any calling involving the handling of 
lead ores, or any of the common lead products is dangerous. Miners, 
painters, plumbers, machinists, and workers in various manufactures 
requiring the use of lead, therefore, most often suffer. The lead is chiefly 
taken in by mouth from unclean hands, but may be inspired, especially 
when men work in poorly ventilated rooms, or may be absorbed from 
the clothing. Water, cider, or wine confined in lead casks or passed 
through new lead pipes may poison. Women are sometimes poisoned 
by hair-dyes or cosmetics containing lead or by biting lead-dyed silk 
thread. 

Morbid Anatomy. — The blue line is found in the margin of the 
gums of the incisor or canine teeth, especially on the lower jaw. It is 
due to a deposit of lead sulphide, formed by combination of lead circu- 
lating in the blood with the sulphur of hydrogen sulphide developed 
from decomposing food. Arteriosclerosis, chronic endocarditis, chronic 
nephritis and gouty lesions may be found. The peripheral nerves show 
degeneration in cases with nerve lesions and the muscles may be atrophic 
and degenerated. The brain may show anemia, edema, and degenerative 
lesions of the cortex. 

Symptoms. — These usually develop after protracted exposure, but 
may present themselves in a few days, if the intoxication is rapid. 
This is most likely to occur in men inhaling fumes heavily charged with 
lead from smelters. The symptoms in some cases develop so rapidly as 
to resemble an acute metallic poisoning ; usually they are evolved slowly, 
and whether of acute or chronic type are of the same general character, 
including (1) Anemia. A secondary anemia with reduction of red cells 
and hemoglobin is present. In addition the blood shows the so-called 
basophilic degeneration of the erythrocytes, the cells showing a fine 
stippling with granules which take up the basic stains. (2) The blue 
line on the gums of the incisor and possibly the canine teeth. It is best 
seen in the lower gums as a fine bluish line in the margin of the gums, 
not removable by cleansing. (3) Lead palsy. Various nerves may be 
involved in the neuritis and several forms of lead palsy are described, 
(a) The wrist-drop or antibrachial type is the most common. When the 
arms are extended the hands droop and cannot be raised, because of 
palsy of the extensors of the wrist. The muscles may atrophy, (b) 
The brachial type, the Duchenne-Erb type, involving the deltoid, biceps, 
and brachialis anticus, sometimes the supra- and infraspinati. (e) 
The Aran-Duchenne type, involving the interossei of the hand and the 
muscles of the thenar and hypothenar eminences, (d) The peroneal 
type, involving the peronei and extensors of the toes, and producing 
foot-drop and the steppage gait, (e) A laryngeal type, iuA^olving the 
adductors of the larynx. Lead palsy is regularly bilateral and s^tii- 
metrical, without sensory sjnnptoms, and accompanied by atrophy. 
Reaction of degeneration is usually present. (4) Colic. Attacks of 
abdominal pain due to spasmodic contraction of the intestine are one 
of the commonest features of lead poisoning. The attacks are mild or 



CHRONIC LEAD POISONING 



303 



so severe as to produce collapse. The pain is regularly referred to the 
umbilical region. Vomiting may occur with severe colic, and the ab- 
domen is found retracted and the muscles rigid. Pressure usually re- 
lieves, but may intensify the pain. The seizures of colic may be repeated 
at short intervals for many days, or may not recur for long periods. 
Dull pain and rigidity of the abdomen may continue between the 
attacks of colic. 

(5) Cerebral symptoms. Encephalopathy. Epileptiform convulsions, 
delirium or coma may occur in severe cases. Transitory, hemiplegia or 
aphasia has been observed. (6) Arteriosclerosis or chronic nephritis 
may be pronounced in advanced cases. The urine regularly contains 
traces of albumin and casts. 

Diagnosis. — Exposure plays such an important role that an occupa- 
tion involving the handling of lead in any form should always excite 
suspicion in a patient suffering from colic or palsy. Confirmation must 
be sought in the presence of the blue line, the basophile degeneration 
of the erythrocytes, which is not pathognomonic, but highly suggestive, 
or the demonstration of lead in the urine by chemical tests. 

Prognosis is regularly good. Some very acute cases are fatal, or 
death may result from protracted poisoning producing arteriosclerosis 
and chronic nephritis. Paralyses usually disappear under protracted 
treatment. 

Treatment. — Prophylaxis is of the greatest practical importance. 
Cleanliness of the hands and person is essential. Ventilation of in- 
dustrial plants, the use of respirators and other hygienic measures have 
greatly reduced the frequency of lead poisoning. Active treatment is 
usually called for by colic, constipation or palsy. For intense colic the 
hypodermic injection of morphine may be necessary. Milder cases may 
be treated by hot applications to the abdomen. The relief of constipa- 
tion is essential. For this purpose magnesium sulphate in dram doses 
is given hourly until the bowels move. Enemata of soap suds or oil 
may also be required. To eliminate lead from the system potassium 
iodide is given in doses of five grains thrice daily, and water is drunk 
freely. The iodide is supposed to act by forming a soluble iodide of 
lead. For the paralysis electricity, either galvanic or faradic, and mas- 
sage are employed. Iron, strychnine and arsenic may be given as gen- 
eral tonics or for the anemia. 

CHRONIC ARSENIC POISONING 

Etiology. — Chronic arsenical poisoning may be caused by the con- 
tinued administration of arsenic for therapeutic purposes in such dis- 
eases as chorea, leukemia and the like. It has been caused by the drink- 
ing of beer contaminated with arsenic derived from the sulphuric acid 
used in manufacturing the glucose entering into the production of the 
beer. Arsenical poisoning is also attributed to the arsenic present in 
dye-stuffs and used for coloring wall-papers, garments of various kinds, 
such as cotton dresses or stockings, playing-cards, etc. The curing of 



304 INTOXICATIONS— MISCELLANEOUS DISEASES 



skins, staining of glass, and the use of Paris green as an insect poison 
are all possible sources of poisoning. Arsenic is said to be regularly 
consumed by the Styrian peasants for the sake of improving the com- 
plexion and bodily vigor. 

Morbid Anatomy. — Various lesions of the skin, pigmentation, 
keratosis, herpes, or urticaria may be found. A degenerative peripheral 
neuritis and granular degeneration of the viscera are regularly present. 

Symptoms. — ^Puffiness of the face, nausea, or vomiting, and head- 
ache are the early symptoms of poisoning noted when the drug is given 
in excessive doses, and regularly cause the withdrawal of the drug. 
Peripheral neuritis and lesions of the skin are the important symptoms 
in more protracted cases of poisoning. The neuritis first affects the 
legs, later the arms or the body generally. Pain in the affected nerves 
is usually present and severe. Paralysis follows, involving especially the 
flexors of the foot, producing foot-drop and the steppage gait. In severe 
cases power and sensation are completely lost in the affected parts. 
The skin lesions are important. Pigmentation of bro^^Tiish tint re- 
sembling that of Addison 's disease may develop. Keratosis of the palms 
and soles, herpes, urticaria or hyperidrosis may be present. 

Course and Prognosis. — If the source of poisoning is discovered 
and the process stopped, the prognosis is regularly good. The neuritis is 
slow and may be protracted, but recovery follows, possibly after months 
of treatment. 

Diagnosis. — Arsenical poisoning must be distinguished from other 
forms of peripheral neuritis, particularly those due to lead and alcohol. 
The arsenical neuritis is marked by sensory disturbances, often severe, 
by the early involvement of the legs, and by the absence of limitation 
to particular muscle groups characteristic of lead palsy. From alcoholic 
neuritis it can be distinguished only by the history of the patient, by 
other evidences of chronic alcoholism, or by proving the presence of 
arsenic in the urine. In any doubtful case appropriate tests should be 
made for this purpose. The source of arsenic must also be sought. 

Treatment. — The source of the drug must be found and its taking 
stopped. Water is given freely to favor elimination. Otherwise the 
treatment is that of peripheral neuritis, rest, with later electricity and 
massage. In the early stages anod^mes may be required. 

FOOD POISONING 

Food poisoning may arise in several ways: (1) from poisons in- 
herent in the food; some edible stuffs are always poisonous, others only 
at certain seasons or under special conditions; (2) from poisons 
produced by fermentation pr decomposition of the food due to bacterial 
action; (8) from infection by pathogenic bacteria or para.sites carried 
in the food, such as typhoid, tubercle, or cholera bacilli, trichina^ or 
the cysticercus. The parasitic infections are discussed elsewhere: (4) 
from metallic poisons contaminating foodstuffs or beverages. Arsenical 



FOOD POISONING 



305 



or lead poisoning may be brought about by food, as already described. 
Canned foods are generally assumed to occasionally cause poisoning by 
tin or solder, but there is little evidence to support the supposition. 
The foods most often the cause of poisoning are fish, meats, milk and 
its products, especially cheese, and some few vegetables. 

Poisons inherent in the food — physiological poisons. Certain fish are 
known to contain substances poisonous to man. Thus in China and 
Japan the ovaries and testicles of a fish called fugu contain a deadly 
poison to which the name fugin is given. Some varieties of fish are 
always poisonous, the tetradon for example, while the organs of others, 
such as the roe of sturgeon, pike, or barbel, are poisonous only in the 
spawning season. Fish which eaten cooked is harmless may be poisonous 
when consumed raw. 

Vegetables are much less likely to be poisonous than the animal 
foods, but certain vegetable poisons are well known, for example the 
muscarin of poisonous mushrooms, ergot, which sometimes contaminates 
rye or other grain, and certain vetches whose seed is used as a substitute 
for wheat. 

Bacterial poisons may be produced in fish, flesh, or milk by bacterial 
action or pathogenic bacteria may be transmitted in food. The develop- 
ment of poisonous substances in food by bacterial action usually accom- 
panies the processes of decomposition. Thorough cooking destroys such 
poisons. Toxalbumins resembling those of diphtheria or tetanus have 
been found in decomposing fish. In other cases the poisons belong to 
the group of ptomaines. Thus from poisonous mussels Brieger isolated 
a ptomaine which he called mytilotoxin, and the tyrotoxin of cheese is 
well known. 

The more frequent food poisonings are due to the presence of patho- 
genic bacteria in the food. The tubercle bacillus, the diphtheria bacillus, 
and the organisms of scarlet or typhoid fever might all be considered 
under this heading, but are elsewhere discussed. The organisms here 
of importance are the bacillus proteus, the bacillus enteridis and a 
variety of organisms belonging in the group of bacillus coli. These 
organisms have been found in food products as the result or the attend- 
ants of disease in fish or meat-animals or as contaminations of food 
products in the course of their handling. Poisoning of either type 
occurs most often from raw or imperfectly cooked food. 

Symptoms. — The disturbances induced by the consumption of food 
products containing toxalbumins or ptomaines produced by bacterial 
action or pathogenic bacteria themselves may be classified in two groups : 
1. Those cases in which the symptoms are those of gastro-intestinal 
irritation, abdominal pain or cramps, nausea and vomiting, and diar- 
rhea with watery stools or stools containing blood and mucus. Fever 
may or may not be present, and may. be of any degree. The accom- 
panying prostration may be slight or may be so severe as to cause death. 

2. Cases in which with or without gastro-intestinal symptoms there 
are marked evidences of disturbance of the central nervous system, such 
20 



306 INTOXICATIONS— MISCELLANEOUS DISEASES 



as headache, delirium, convulsions or even coma; vertigo and stagger- 
ing gait; dryness of the throat and difficulty in swallowing; salivation; 
visual disturbances with imperfect vision, sometimes blindness, dilata- 
tion of the pupils, and paralysis of ocular muscles or ptosis; great 
muscular exhaustion and prostration. Disturbances of sensation of 
various kinds and loss of power in the extremities have been observed. 
The disturbances of this class may also be slight or may be extreme and 
death may follow. Convalescence in either of these groups is often slow 
and difficult. 

Vegetable poisons such as muscarin may also produce symptoms of 
the same character as those described above; in most cases, however, the 
intoxication is more slowly developed, the clinical symptoms are of more 
chronic type and malnutrition is pronounced. 1. Ergotism is due to 
meal or flour made from grain contaminated by the fungus claviceps 
purpurea. Two types are recognized: (a) Gangrenous, attributed to 
sphacelinic acid. The marked feature is malnutrition with gangrene of 
the fingers, toes, ears or nose, (b) Nervous, attributed to cornutin. 
Headache and weakness appear early, to be followed by muscular cramps 
and contractions. The spasms recur at various intervals and last for 
hours or days. Delirium, melancholia, or insanity may follow. 

2. Lathyrism is due to the adulteration of flour with the chick-pea 
vetch. It is unknown here, but occurs in parts of Europe and Asia. 
The symptoms resemble those of the convulsive type of ergotism. 

3. Pellagra is a poisoning due to eating fermented unripe maize or 
Indian corn. Many cases have recently been observed in the United 
States. The symptoms include indigestion, insomnia, salivation and 
diarrhea and an erythematous eruption followed by marked dryness of 
the skin and desquamation or the development of furuncles, severe 
nervous disturbances, such as gradual paralysis of the legs, melancholia, 
or suicidal mania. Death may result. (See p. 420.) 

Diagnosis. — Pood poisoning usually presents itself in a group of 
people who have partaken of food together, or in institutions where the 
inmates have the same diet. In individual instances the relation of the 
disturbances to the taking of food, often noted to have been tainted or 
decomposed, is suggestive. From the clinical symptoms the food may 
be brought under suspicion. The nature of the poison, whether bacterial 
or chemical, can be determined only by the careful bacteriological or 
chemical analyses. In the chronic vegetable intoxications evidence must 
be sought of the contamination of the food and the results of a change 
to a healthy diet tried. 

Treatment. — In bacterial poisonings the indications are to empty the 
alimentary tract by purges or by washing out the stomach and irrigating 
the colon. Stimulants may be required for the prostration, and morphine 
for the relief of pains or diarrhea. Careful feeding and tonics will be 
required in convalescence. In acute intoxication with vegetable poisons 
(muscarin) like measures may be indicated. In the more chronic t;^^es 
mentioned above the chief requirement is a change of diet. 



CARBONIC MONOXIDE POISONING 



307 



CARBONIC MONOXIDE POISONING 
(Illuminating Gas Poisoning) 

Poisoning by pure carbon monoxide is too rare to be of practical 
importance, but this carbon compound is the most dangerous com- 
ponent of illuminating gas, and also of the gases of combustion which 
rise from furnaces, charcoal braziers, and the electrical furnace. 

Etiology. — Accidental poisoning occurs occasionally in those working 
about furnaces, or the charcoal braziers, or from illuminating gas. The 
great majority of cases result from the inhalation of illuminating gas 
accidentally or with suicidal intent. 

Morbid Anatomy. — The surface of the body is often marked by 
irregular areas of a cherry-red staining, and there is much post-mortem 
discoloration. Bronchitis, bronchopneumonia or lobar pneumonia is 
usually present. The pia mater and brain are congested, and in cases 
which have survived five or six days a very remarkable softening of 
the globus pallidus of the lenticular nucleus is found. Nephritis may 
be found. 

Symptoms. — Headache, mental dulness, dyspnea, cyanosis, and pros- 
tration are produced in the milder cases of poisoning. In severer cases 
the victims are found comatose, the skin and mucous membranes deeply 
cyanotic, the pupils contracted, the conjunctivae bloodshot, the pulse 
rapid, bounding and weak, the respiration rapid and labored. The 
temperature is often raised to 103°-104° F. The patients may die in a 
few hours, with rising temperature and failing pulse, or they may 
gradually recover. The cherry-red staining of irregular areas of the 
skin is often seen during life, and the drawn blood has the same color. 
Marked rigidity of the extremities may be present. The fever often 
continues high, irrespective of complications, such as broncho- or lobar 
pneumonia, which would account for it. The urine is scanty and contains 
albumin and casts. Those who recover are liable to suffer for indefinite 
periods from vague nervous disturbances. 

Prognosis is always grave, but recoveries occur even after coma 
lasting for days. In protracted cases broncho- or lobar pneumonia 
usually develops. 

Treatment. — Fresh air is the first requirement and may be sufficient 
to revive the mild cases. For the severer cases free bleeding with the 
subsequent intravenous injection of normal salt solution 1000 c.c. is 
helpful. Oxygen may be administered. Direct transfusion is indicated 
and may succeed in desperate cases. The reactions of the two bloods 
should be first tested to be sure that hemolysis does not take place on 
their mixture. Cardiac and respiratory stimulants are usually required. 
Feeding must often be carried out by nutrient enemata or by the nasal 
tube. 



308 



INTOXICATIONS— MISCELLANEOUS DISEASES 



SUNSTROKE 

(Insolation. Thermic Fever. Siriasis) 

Definition. — A morbid condition induced by exposure to extreme 
heat. 

Etiology. — (1) Exposure to high temperatures of any kind may 
produce prostration. The beat of the sun's rays is the most common 
cause and produces the severest tj'pe of sunstroke, but similar conditions 
result from hig-h temperatures in-doors, as in boiler-rooms, about 
furnaces, or in bakeries. (2) Predisposing causes include especially the 
excessive use of alcohol, and any cause for debility. (3) The loss of 
sleep incident to protracted hot weather, and hard labor are also 
important influences. 

Morbid Anatomy. — There is a general venous congestion of the skin 
and internal organs and small hemorrhages may be found in the skin 
or serous membranes. The brain is congested and under the micro- 
scope degenerative lesions resembling those produced by intoxications 
with alcohol, lead, etc., are found. These are the most characteristic 
lesions. 

Symptoms. — These vary greatly under different conditions and 
much confusion exists as to the terminology applied to different clinical 
conditions. The subject "will be best understood by considering that the 
conditions described result from exposure to heat, either of the sun or 
from other sources, that they are doubtless degrees in one process and 
that anomalous cases, or cases not falling easily into any group of the 
classification may be seen. 

(1) Heat Exhaustion. — This condition is seen most often in those 
working in-doors under high temperatures, firemen, bakers, laundresses 
or cooks and the like. The patient is prostrated, the surface usually 
pale and clammy, the pulse soft and of normal rate or but little quick- 
ened. The mind is perfectly clear, though headache may be complained of. 
The temperature is normal or subnormal. 

(2) Sunstroke. — This is commonly the result of working in the 
direct rays of the sun, but not always. Premonitory symptoms of 
headache, dizziness, dryness of the skin may be present, or the ^dctim 
msj fall unconscious without warning. 

In the milder cases prostration is marked, the temperature is raised 
to a varying degree, 101° to 105° F., the pulse is rapid and feeble. The 
skin is cool and moist. There are headache, vertigo, and possibly mild 
delirium, but not coma. Nausea or vomiting may occur. Eecovery is the 
rule. 

In the severe cases the patient passes suddenly into coma, the face 
and skin generally are flushed, dry, and burning hot, the pupils are 
normal or contracted, the extremities are sometimes rigid, sometimes 
flaccid, not infrequently convulsions occur, and urine and feces are 
discharged involuntarily. The temperature ranges from 105° to 115° F., 
the pulse is very rapid, and correspondingly weak, the respiration is 



DISEASES OF THE MUSCLES 



309 



rapid and noisy, the lips and finger-nails are cyanotic. Unless relieved 
by prompt treatment the patient dies in a few hours. In those recover- 
ing under treatment the temperature falls rapidly, consciousness returns 
m part at least, the pulse improves and the patient gradually returns to 
a normal condition. Secondary rises of temperature with stupor or 
coma and other manifestations of the primary stroke may occur. Coma 
may last for days. 

Diagnosis. — The conditions under which the prostration occurs 
usually render diagnosis easy. The absence of other causes for pros- 
tration, such as heart failure, is important. In the febrile cases severe 
malarial paroxysms may be overlooked. The enlarged spleen and the 
examination of the blood should prevent error. 

Prognosis. — The milder cases recover. ' Of the severer ones, those 
with temperatures of 105° or over, the mortality will reach 10 per cent. 

Treatment. — For heat exhaustion and the milder cases of sunstroke, 
rest in a cool and quiet room, with a sponge bath if the temperature be 
high, and moderate stimulation by whiskey or brandy, is all that is re- 
quired. For severe sunstroke the patient is stripped and either rubbed 
with cakes of ice or put in an iced bath. A thermometer is kept in the 
rectum and when the temperature has fallen to 105° or 104° the rubbing 
or bath is stopped. The temperature continues to fall to normal or 
even below. Camphor and ether, caffeine, strychnine, or other cardiac 
stimulants are given hypodermatically, if the pulse fails. The tem- 
perature must be watched and a cold bath given, if it begins to rise 
again. When these methods cannot be carried out, douching the body 
with cold water may be tried. 

DISEASES OF THE MUSCLES 

MYOSITIS 

Myositis occurs in some forms of muscular rheumatism, in trichiniasis, 
and in pyemia, or in localized abscesses. Otherwise myositis is a rare 
affection. It has, however, been encountered and described under several 
different forms. 

(1) Primary Suppurative Myositis. — This affection is seen fre- 
quently in Japan. There are multiple localized areas of induration in 
the muscles, and abscesses are often found. Pyogenic bacteria are found 
in the abscesses. The constitutional symptoms are those of pyemic 
infection, and the possibility of a cryptogenic pyemia can hardly be 
excluded. 

(2) Dermatomyositis.— This is an acute, sub-acute or chronic 
disease, of unknown etiology, characterized by a gradual onset of local- 
ized areas of edema, dermatitis and myositis. The morbid anatomy 
consists in a definite myositis with swelling of the muscle, edema, infiltra- 
tion wath leukocytes and degeneration of the muscle fibers. Hemor- 
rhages may be found in the muscles. 



310 INTOXICATIONS— MISCELLANEOUS DISEASES 



Symptoms. — Vague pains throughout the body mark the onset, 
later the pains become so severe that the patient is bed-ridden. Fever, 
perspiration, and enlargement of the spleen are observed. Then areas 
of edema and dermatitis overlying the inflamed muscle develop on 
various non-symmetrical parts of the body. Stomatitis and angina 
develop in some cases and involvement of the muscles of deglutition and 
respiration often lead to death from suffocation or bronchopneumonia. 

The course of the disease may be very acute, one to two weeks, or 
ver}'- chronic, as many years. More than half the reported cases resulted 
fatally. 

Treatment must be directed to the relief of pain and the mainte- 
nance of nutrition. 

Myositis Ossificans. — This is a very rare disease, seen occasionally 
in boys at puberty. Areas of myositis develop which after a time sub- 
side, leaving areas of connective tissue formation in which cartilage 
and bone are ultimately deposited. The process therefore results in 
gradual deposition of these substances in various muscles throughout 
the body, leading in the end to great disability and pseudo-ankylosis 
of joints. The temporals, pterygoids and masseters are finally involved 
and the patient is unable to open his mouth or masticate his food. 
Exostoses are common. The disease lasts for many years. The subjects 
die from intercurrent infections. Many medicines have been used with- 
out result. Operative measures may be necessary. 

MYOTONIA CONGENITA 
(Thomsen's Disease) 

Definition. — A congenital nervous affection characterized by muscular 
cramps at the beginning of voluntary movements. 

Etiology. — The disease occurs in certain families. ConsangTiinity is 
thought to be a factor. Fright or injury sometimes precedes the 
development of symptoms. Males are more often affected. 

Morbid Anatomy. — Sections of muscle examined during life have 
sho\^Ti an increase in the nuclei in the muscle fibers, an increased width 
of the fibers and various modifications of their protoplasm. The latter 
may show vacuolation, disappearance of normal striation, fibrillation, 
or other degenerative changes. These changes are probably the results 
rather than the causes of the disease. 

Symptoms. — These commonly develop above the age of 20, but may 
appear during childhood or puberty. Military service has first brought 
them out in a number of cases. Tonic cramps, without pain, develop 
in the muscles on attempting any voluntary movement. The cramps 
recur several times on the repetition of the effort and then vanish, so 
that the muscles can be used normally. The result is a certain awkward- 
ness in the performance of any movement till the cramps have passed 
off. All the voluntary muscles may be affected, and the difficulty ap- 
pears in walking, shaking hands, speaking or eating. In some instances 



DISEASES OF THE MUSCLES 



311 



a single group of muscles is involved. The muscular contractions are 
slow, weak, and last some time after the effort which excites them. The 
muscles become hypertrophied and the patient looks strong, but is 
actually below normal in power. The persistence of the contractions 
after electrical stimulation is the chief feature of these reactions. 
Tendon reflexes are normal, deficient or increased. 

The disease varies from mild to severe grades, is chronic and in- 
curable. No effective treatment has been found. 

MYASTHENIA GRAVIS 
(Asthenic Bulbar Paralysis) 

Definition. — A disease characterized by signs of extreme muscular 
fatigue, without definite lesions of either nervous or muscular system. 

Etiology. — The disease commonly develops between the ages of 
twenty and thirty, but has been observed in infancy and old age. 

Previous acute disease, menstruation, pregnancy, and the menopause 
apparent!}^ bring out the sjTuptoms, but can hardly be regarded as 
causing the disease. 

Morbid Anatomy. — The nervous system is normal; the muscles 
may show an infiltration of lymphocytes between the muscle fibers. 

Symptoms. — The onset is slow, insidious. The evidences of the 
disease usually appear first in the muscles of the eyes, the jaws or 
lips. Ptosis, diplopia, and difficulty in mastication are therefore early 
symptoms. The ptosis or other symptoms disappear after rest or sleep, 
to recur on any effort and finally become permanent. All the muscles 
of the body may finally be affected. The muscles of respiration are 
involved in the terminal stage, causing dyspnea and ending in broncho- 
pneumonia. 

Myasthenic Reaction. — A faradic current applied to affected muscle 
excites a strong contraction, which, however, soon lessens, till finally there 
is no response. The same early fatigue can be demonstrated by the 
attempt voluntarily to repeat a given muscular contraction, such as 
closing the eye, chewing or whistling. The muscles quickly fail and 
can only be made to act again after rest. The reflexes are exaggerated. 
Sensory symptoms are lacking. The diagnosis is easy, if the symptoms 
are borne in mind and the muscles tested by electricity and voluntary 
action. The disease in its early stages is often mistaken for hysteria. 

Many cases result fatally ; recovery is possible. Prolonged rest with 
systemic tonics constitute the treatment. 

PARAMYOCLONUS MULTIPLEX 

A nervous affection characterized by clonic lightning-like contractions 
of the muscles, usually those of the lower extremities. The etiology and 
pathology are obscure. The affected muscles, the vastus, rectus, or 
adductors, or, in the arm, the biceps, triceps, or supinator longus, con- 



312 INTOXICATIONS— MISCELLANEOUS DISEASES 



tract swiftly as though electrically stimulated, but, as a rule, no move- 
ment results. 

The electrical reactions are normal. The contractions may be in- 
creased by mechanical irritation of the skin or the muscles themselves. 
Treatment must be directed to the general condition of the patient. 

RARE DISEASES OF THE BONES AND JOINTS 
(Osteitis Deformans, or Paget's Disease) 

Definition. — A rare chronic disease of the skeleton characterized 
by enlargement of the cranial vault and forward projection of the head 
with dorso-cervical kyphosis, prominence of the clavicles, widening of 
the base of the thorax, a relative increase in the width of the hips and 
a forward bowing of the legs. The etiology is unknown. It appears 
sometimes to be closely associated with the growth of malignant tumors, 
carcinoma or sarcoma. 

The morbid anatomy combines hypertrophic and rarefying osteitis. 

The s^Tnptoms consist of the bony changes and irregular shifting 
pains, possibly headache. The shortening of stature from bowing of 
the spine and legs may amount to a foot or more. The disease is 
progressive, but the patients die of intercurrent infections. 

Leontiasis ossea is perhaps a variety of Paget's disease affecting 
particularh' the bones of the head and face. The steady increase in 
the size of the head is the striking feature of the affection. Headache, 
insomnia, apathy, mental dulness, or epilepsy may be associated Avith 
the bony changes. The condition may later develop into Paget's disease. 

Hypertrophic pulmon.miy osteoarthropathy is an enlargement of 
the bones and to some extent of the soft tissues of the extremities, 
especially the fingers and toes. The enlargement is symmetrical. (See 
Fig. 1.) In the fingers and toes the increased size is due to hypertrophy 
of the soft parts. In the arm or leg there may be marked thickening of 
the distal ends of the long bones. Occasionally effusions into the joints 
are found. The condition is closely associated with chronic pulmonary 
disease, especially bronchiectasis, but is often seen in congenital heart 
disease and a variety of other affections. 



VIII. 



THE INFECTIOUS DISEASES 

TYPHOID FEVER 
(Enteric Fever. Typhus Abdominalis) 

Definition. — Typhoid fever is an acute general infection due to a 
specific micro-organism — the hacillus typhosus — marked by character- 
istic lesions in the intestinal lymph follicles and elsewhere, and manifested 
clinically by protracted fever, prostration, intestinal disturbances, en- 
largement of the spleen and a rose-colored skin eruption. 

Etiology. — Typhoid fever is one of the most widely distributed of 
the infectious diseases. Although its greatest prevalence is in temperate 
regions it seems little affected by climate or altitude, nor do races show 
much difference in susceptibility. It is more common in cities than 
in the country and occurs both endemically and in small, local epidemics. 
Its prevalence in a community bears a direct relation usually to con- 
ditions of sanitation, and especially to the purity of the water supply. 

Season. — The disease prevails chiefly in the late summer and autumn. 
Considerably more than half of the cases occur during the months of 
August, September, October and November. A hot, dry summer seems 
to have some influence in augmenting the number of cases. 

Age. — Typhoid fever is chiefly a disease of young adult life. Lieber- 
meister 's statistics showed that 58 per cent, of the cases occurred between 
the age of 20 and 30 years. It is not uncommon in older children and 
in middle life, but cases are extremely, rare in infants under one year 
and in old age. 

Sex. — Males seem slightly more liable to attack than females. 

Condition of Health. — It has long been noticed that the disease is es- 
pecially prone to attack the vigorous and well-nourished individuals rather 
than the weakly. The well-to-do suffer equally with the poor. Preg- 
nancy, the puerperal state, lactation and certain of the infectious diseases 
seem rather to diminish susceptibility to the disease (Curschmann) . 

Immunity. — Variations in individual susceptibility doubtless exist. 
One attack usually confers immunity, but two and even three attacks 
in the same person have been observed. 

Bacteriology. — The direct, exciting cause of typhoid fever is a 
specific micro-organism — the bacillus typhosus, discovered in 1880 by 
Eberth and carefully studied by Gaffky and others. It is a short, rather 
thick, flagellated, actively motile rod whose length is one-third of the 
diameter of a red cell. It grows readily on most of the usual culture 
media and does not form spores. 

In the body the bacilli are found abundantly in the intestinal lesions, 
the mesenteric lymph-nodes, the spleen and, less constantly, in the bone 
marrow, liver, gall-bladder and other organs. Recently, by improved 

313 



314 



THE INFECTIOUS DISEASES 



methods, they have been isolated from the circulating blood in about 
three-fourths of all the cases examined. They have also frequently 
been demonstrated in the rose spots. In the stools of patients the germs 
are found ahnost constantly in great abundance. In a certain proportion 
of cases (20-30 per cent.), moreover, they are found abundantly in the 
urine. These are the two chief avenues by which the bacilli leave the 
body and by which transmission of the disease occurs. The sputum rarely 
contains the bacteria and the sweat and expired air probably never. 

Outside of the body typhoid bacilli may, under even moderately 
favorable conditions, live and remain active for weeks and months. 
They are readily destroyed by even weak solutions of such germicides 
as carbolic acid and the bichloride of mercury and by exposure for 
fifteen minutes to a temperature of 60° C. On the other hand, they 
are very tolerant of cold and may retain their vitality when kept in 
ice for as long as three months. 

Exposure to direct sunlight will destroy them in a few hours. They 
are known to live in fecal matter, water, earth, and even dust, for at 
least many weeks. Whether under such circumstances they are capable 
of multiplication is still uncertain. 

Transmission. — Typhoid fever may be contagious in the usual mean- 
ing of the term. That the germs enter the body, in the vast majority 
of cases, through the alimentary tract cannot be doubted. Indeed, evi- 
dence is lacking that infection ever occurs by any other channel. 

Contaminated drinking water is by far the most important mediiun 
of infection. Streams, reservoirs, wells, springs, exposed to pollution 
from typhoid discharges by means of surface drainage or from neigh- 
boring cesspools, are the usual sources. 

A number of epidemics have been traced to milk, infected by con- 
taminated water. Oysters fattened at the mouth of polluted streams 
have been shown to be the source of at least several small epidemics. 
The transference of infectious material by flies and other insects de- 
serves greater attention than it has hitherto received. Where cesspools 
are exposed and open, as in the country districts and especially in army 
camps, this means of infection is probably often an important one. 
Nurses and attendants upon typhoid patients occasionally infect them- 
selves through lack of care in handling bedpans^ soiled linen, etc. 

Of recent years typhoid bacilli have been repeatedly found in the 
feces of persons who had had the fever months or years before, and in 
some instances in those who had never had the fever, and localized 
epidemics have been traced to direct infection from such " carriers " 
employed as cooks or the like. 

Morbid Anatomy. — The essential lesions of typhoid fever are found 
in the lymph tissue of the intestines, the mesenteric lymph-nodes and 
the spleen. 

Intestines. — The lymph tissue of the intestines is made up of 
solitary follicles, which are scattered widely through small intestine, 
vermiform appendix and colon; and Peyer's patches, which are aggre- 



TYPHOID FEVER 



315 



gations of solitary follicles occurring chiefly in the ileum. Although 
these structures are liable to involvement everywhere throughout the 
length of the intestines the lesions are regularly most numerous and 
extensive in the lower part of the ileum, w^here the lymphoid tissue is 
most abundant. 

The changes taking place in both the Peyer's patches and the solitary 
follicles are identical in character and may conveniently be divided 
into several stages. 

(1) Congestion and hyperplasia. 

(2) Necrosis and sloughing. 

(3) Ulceration, 

(4) Cicatrization. 

1. Congestion and Hyperplasia. — The glands affected are of reddish 
gray color and are swollen and somewhat raised above the surrounding 
mucous surface ; the solitary follicles varying in size from that of small 
shot to that of a pea. Microscopically there is at first hyperemia fol- 
lowed by a great increase of the lymphoid cells of the gland (" medullary 
infiltration "). As this hyperemia increases the blood-vessels are com- 
pressed and the patch becomes grayish white in color. Early in the 
second week of the disease the hyperplasia of the gland usually reaches 
its height and now involution may occur in one of two ways. In the 
milder cases the accumulated cells of most of the glands undergo 
degeneration and absorption and the gland soon regains its normal 
state. More commonly, however, most of the glands undergo — 

(2) Necrosis and Sloughing. — This necrosis is due in part to the 
compression of the blood-vessels (anemic necrosis), and in part, probably, 
to the action of the toxins of the typhoid bacilli. The necrosis may 
involve only a small part of a gland, or the entire surface of a patch may 
die and form a slough. 

(3) Ulceration. — From the separation of these sloughs there result 
the idcers which are the most conspicuous feature of the typhoid lesions. 
They correspond in position, of course, to the affected Peyer's patches 
and solitary follicles, but are by no means always co-extensive \^dth the 
limits of these glands. Usually, indeed, they occupy only a portion of 
the surface of such glands. Their outlines may be round, oval or quite 
irregular. Their edges are usually sharp and clean cut. In depth they 
vary exceedingly. Some are so shallow as to involve only the superficial 
layers of the mucosa. Usually they extend to the submucous or muscular 
layer, occasionally they penetrate to the peritoneal coat or even per- 
forate the entire wall. This latter event with its consequent septic 
peritonitis constitute;^ one of the gravest of the complications of the dis- 
ease. Moreover, the separation of the sloughs and the development of the 
ulcers often result in the erosion of blood-vessels and free hemorrhage 
into the intestine. Ulceration is usually most extensive in that part of the 
ileum immediately above the ileo-cecal valve, as it is here that Peyer's 
patches are largest and most numerous. The stage of ulceration occupies 
usually the latter half of the second and third weeks of the illness. 



316 



THE INFECTIOUS DISEASES 



(4) Cicatrisation. — In ordinary cases the process of healing begins 
almost as soon as the ulcers are well developed. The loss of substance 
is gradually filled up by granulation tissue, the epithelium extends over 
from the edge of the ulcer and a scar results, which in the course of 
time becomes somewhat depressed and often pigmented. Such scars, 
however, rarely produce serious constriction of the bowel. The healing 
process is usually well under way by the beginning of the fourth week. 
Sometimes, however, when the recuperative power is small, healing may 
be delayed for many days. 

In addition to the specific lesions mentioned, both small and large 
intestine are usually the seat of more or less extensive catarrhal inflam- 
mation to which, rather than to the change in the lymph follicles, are 
attributed certain of the intestinal symptoms and in particular the char- 
acteristic "pea-soup" stools. The ulceration may extend into the colon 
and even become extensive there. 

Typhoid Fever Without Intestinal Lesions. — The severity of the 
symptoms by no means always corresponds with that of the intestinal 
lesions. In some cases these latter may be very slight and inconspicuous. 
Indeed, in a few fatal cases recently reported no characteristic intestinal 
changes whatever could be found, although typhoid bacilli were isolated 
from the blood and organs. 

The Mesenteric Lymph-Nodes. — The same process of lymphoid 
hyperplasia is seen in the lymph-nodes of the mesentery, especially in 
those of that part of the mesentery which is opposite to the site of the 
chief intestinal lesions. The nodes are much swollen and may be seen 
in the mesentery at autopsy as nodules, often as large as a cherry. In 
these extensive necrosis is much less common than in the intestinal 
follicles, although small foci of necrosis are not infrequent. Usually the 
medullary infiltration undergoes absorption and resolution and the 
nodes return to normal with the subsidence of the intestinal lesions. If, 
as happens occasionally, these swollen nodes are secondarily infected by 
pyogenic organisms, suppuration and abscess may result. Even the 
retroperitoneal nodes may share in the swelling and hyperplasia. 

The Spleen. — The enlargement of the spleen occurs early and con- 
stantly. At autopsy it is found usually to be from li/o to 3 times its 
normal size. This increase depends upon its engorgement with blood 
and upon the marked hyperplasia of its lymphoid elements. It is usually 
dark red or bro^^Tlish in color and soft or even diffluent in consistency. 
Occasionally it is the seat of infarct or abscess. Spontaneous rupture has 
occurred. 

Other Lesions. — The liver shows constantly a greater or less degree 
of degeneration, albuminous or fatty, of the hepatic cells. Frequently 
also minute foci of hmiphoid cells are found scattered through it which 
may undergo necrosis. Liver abscess is a somewhat rare complication. 

Inflammation of the gall-hlachler and large hile-flucts is not uncommon. 

Heart. — The myocardium is frequently involved and shows two types 
of lesions — (1) a degeneration of the muscle fibers, pare ncliyniatous dc- 



TYPHOID FEVER 



317 



generation; and (2) an exudative inflammation of the interstitial con- 
nective tissue — acute myocarditis. Endocarditis and pericarditis are rare. 

Blood- Vessels. — Thrombosis of an artery with consequent gangrene 
of the part is rarely seen. A similar thrombosis of the large veins, espe- 
cially of the femoral, is less uncommon. It depends upon an inflamma- 
tion of the vein wall (phlebitis) caused, in some cases at least, by the 
typhoid bacilli themselves. 

The larynx is very commonly the seat of a catarrhal laryngitis. 
Occasionally a severer type of inflammation with ulceration and even 
with destruction of the cartilages is found. 

Lungs. — In the lungs a great variety of lesions occur. Lobar and 
lobular pneumonia, gangrene, abscess and hemorrhagic infarction are 
all occasionally seen. The role of the typhoid bacilli in these processes 
is still unsettled. Frequently, at least, they are due to infection by 
other bacteria. Hypostatic congestion is often found in the fatal cases. 
Fibrinous or serous pleurisy is not of very frequent occurrence. In 
some of these cases, and in the rare cases of empyema, typhoid bacilli in 
pure culture have been found. 

Kidneys. — Parenchymatous degeneration of varying degree is the 
rule and in fatal cases true acute nephritis is not infrequently met with. 
Catarrhal and suppurative inflanmiations of the pelvis of the kidney and 
of the bladder, due to the bacillus typhosus, occur. 

Among the rare lesions found are acute leptomeningitis, parotitis, 
periostitis, osteomyelitis and joint inflammations. The voluntary mus- 
cles, especially those of the abdomen, show not infrequently a peculiar 
type of degeneration which sometimes results in hemorrhage or spon- 
taneous rupture. 

Symptomatology. — It will be convenient to give first a general de- 
scription of the symptoms and course of the disease in its typical form 
and in the common variations from this, and to take up later in detail 
the individual symptoms and complications. 

Period of Incubation. — In infectious diseases the time elapsing be- 
tween the entrance of the specific germs and the manifestations of the 
first definite symptoms is known as the period of incubation. In typhoid 
fever this period is less easy to estimate accurately than in the case of 
contagious diseases such as the exanthemata. Usually, however, it 
varies between one and two weeks. Occasionally it is as much as three 
weeks and it may be even longer. This period is often quite free from 
symptoms, but not infrequently there are noticed vague discomfort, lan- 
guor and failing appetite. 

Course and General Description. — The acute stage of the disease 
commonly lasts from three to five weeks, the first day of fever usually 
being counted the first day of the disease. 

Onset. — First Week. — The onset is almost always insidious and grad- 
ual. Lassitude, loss of appetite, headache, pain in the back and legs, 
fever and chilliness are the symptoms usually complained of. A distinct 
rigor is uncommon. The headache is usually frontal and is often severe 



318 



THE INFECTIOUS DISEASES 



and persistent. It is, however, by no means always present. Epistaxis 
is common. The face is flushed: the tongue usually small, moist, coated 
with a yellow or whitish fur and often clean and red at the edges and 
tip. There may be nausea and vomiting. Constipation is the rule, but 
mild diarrhea may be present from the beginning. The abdomen is 
soft and tenderness is slight or lacking. The fever usually rises from 
day to day and at the end of the first week may reach 104°-105° F. The 
pulse is slightly accelerated (80-100), full, of low tension and some- 
times dicrotic. A mild grade of pharj^ngitis, laryngitis or bronchitis 
is of very common occurrence. 

Second Week. — The fever reaches its height usually before the 
beginning of the second week and continues high throughout the week. 
All the evidences of continued fever are now marked. The tongue and 
lips are dry, the face is flushed but heavy and apathetic. The patient 
is apt to sleep most of the time, but the sleep is restless and troubled. 
If delirium be present it is usually of the quiet, muttering type. The 
pulse is somewhat more rapid and less strong. At the beginning of 
this week or at the end of the first week two symptoms of great diag- 
nostic importance usually appear: (a) the eruption of rose-spots upon 
the abdomen (7th to 9th day) and (b) the distinct enlargement of the 
spleen. Tympanites and diarrhea are common. Intestinal hemorrhage 
may occur. Death may result during this week from severe nervous 
disturbance or from early complications. 

Third Week. — In mild cases this week may mark the beginning of 
convalescence. In the average cases, however, it is the critical period 
of the disease; the time when intestinal ulceration is most extensive, 
when the danger of hemorrhage and perforation is greatest and when 
complications, especially pulmonary ones, are most likely to develop. 
The temperature still continues high, although less uniformly so. The 
patient lies constantly upon his back, completely prostrated, anemic 
and emaciated. The tongue is dry and cracked, the teeth and lips covered 
^vith sordes. Tympanites and diarrhea are common. IMental apathy is 
extreme. There is apt to be stupor or quiet delirium. The heart action 
is rapid and feeble, the skin pale and the extremities often slightly 
cyanotic. Toward the end of the week, in favorable cases, the tempera- 
ture begins to fall and the evidences of toxemia become less marked. 

In the fourth iceek, in such cases, the temperature gradually falls 
to normal, the patient grows brighter and the heart action stronger. 
The tongue again becomes moist and the appetite returns, but prostra- 
tion and emaciation are still marked. In protracted cases the features 
of the third week are continued into the fourth or even into the eighth 
or ninth week of the disease. 

Convalescence, even if uninterrupted by complications or relapses, is 
slow and tedious. The regaining of the lost flesh (often 30 or 40 
pounds) requires usually several weeks at least and the return of 
strength is no more rapid. 

Variations. — 1. In IMode of Onset. — Instead of the usual 
insidious onset the disease may begin in one of the following ways: 



TYPHOID FEVER 



319 



(a) Suddenly with one or more chills and with an abrupt rise of 
temperature. 

(b) With persistent and uncontrollable vomiting, either with or 
without severe diarrhea. 

(c) With pronounced pidmonary symptoms. These are most com- 
monly symptoms of a severe and general bronchitis. Occasionall}^, 
however, the disease begins with the symptoms and signs of a lobar 
pneumonia and its true nature may not be evident for some days — the 
so-called ' ' pneumo-typhoid. ' ' 

(d) With severe nervous sj^mptoms. Intense headache, insomnia, 
neuralgic pains, photophobia, delirium, even retraction of the head and 
convulsions, may be present in varying combinations. The symptoms 
may for some days closely simulate meningitis. 

(e) With symptoms of an acute nephritis — " nephrotyphoid. " 

2. In Cours e. — Departures from the course above described are 
numerous and varied. There are, 

(a) Mild cases, in which all the symptoms, including the tempera- 
ture, are relatively slight and in which the course is usually short (ten 
days to three weeks). 

(b) Protracted cases usually, but not always, severe, in which the 
fever and the other symptoms, even when uncomplicated, may continue 
for five, six or even nine weeks. 

(c) Malignant or Fulminant Typhoid. — In which from beginning 
the infection is very intense, the temperature very high and the heart 
action rapid and feeble. Such cases may be fatal even in the second 
week. 

(d) Abortive Typhoid. — In which after the usual onset, or one more 
abrupt than usual, the disease is interrupted at the beginning, middle 
or end of the second week by a rapid, or even critical, defervescence and 
a speedy recovery. Such cases are by no means always mild ones. 

(e) Ambulatory Typhoid (''Walking Typhoid"). — An important 
and not uncommon class of cases in which during the early stage the 
patient has not felt sick enough to go to bed, but has kept about and 
perhaps at work. Such cases often first come under observation during 
the second week or even later. They may apply for treatment only 
when intestinal hemorrhage or perforation has occurred. 

(f) Hemorrhagic Typhoid. — Rare eases, often fatal, marked by 
development of purpuric symptoms such as hemorrhage beneath the 
skin, from the mucous membrane and into the viscera. 

In Child re n. — The disease in children is apt to run a somewhat 
shorter and milder course than in adults. The fever is often of a more 
distinctly remittent type, prostration is less pronounced and the severe 
intestinal complications of hemorrhage and perforation less common. 
On the other hand, relapses are of distinctly greater frequency. The 
mortality is very low. 

In the Age d. — Typhoid fever is marked by a tendency to early 
and great prostration, cardiac depression, delirium and fatal pulmonary 
complications. 



320 



THE INFECTIOUS DISEASES 



Afebrile Typhoi d. — Cases of typhoid infection without fever 
occur, but are extremely rare. Convalescent patients may show bacilli 
in the feces for years. Occasionally the bacilli are found in those who 
have never had the fever. 

Individual Symptoms. — Fever. — The course of the fever may be 
conveniently divided into three stages: the initial rise, the period of 
febrile elevation or fastigium, and the period of defervescence. The 
initial rise occupies from four to six days. There is usually a step-like 
increase from day to day, the fever each evening being one or one and 
a half degrees higher than that of the evening before. This same in- 
crease is to be seen also in the morning temperature, which, however, is 
regularly from one and a half to two degrees lower than that of the 
evening of the same day. This initial rise is sometimes much more 
abrupt and may occupy only two days or even less. (See Fig. 61.) 




Fig. 61. — Temperature of typhoid fever, showing the gradual rise, the fastigium or height of the fever, 
and the fall by lysis. A normal course of three weeks. 



The fastigium or stage of febrile elevation 
occupies, in typical cases, the second and third wrecks of the disease. Dur- 
ing this time the fever maintains a fairly constant elevation varying from 
103° to 105° F., the morning remissions being gradually not more than 
one degree. In the milder cases the temperature may reach only 102° or 
1021/^°. Occasionally in severe types it rises to 106° or even more. The 
duration of this stage varies greatly. In many of the cases it is not 
longer than one week. In the protracted cases it may be three, four or 
even six weeks in extent. In the latter part of this stage the morning 
remissions are generally increased to two or even three degrees, while the 
evening temperature still maintains its height. The increased drop in 
the morning temperature is usually the first sign of beginning deferves- 
cence. Sudden, violent drops in temperature are uncommon except as 
the result of severe intestinal hemorrhage, perforation or profuse sweat- 
ing. Occasionally, however, the fever may be markedly remittent 
throughout. 

The stage of defervescence is usually of about one 
week's duration. During this time the temperature gradually falls to 



TYPHOID FEVER 



321 



normal, the evening rise being the last to disappear. Following this there 
are usually a few days of slightly sub-normal temperature. Many varia- 
tions from the course described are seen in the stage of defervescence. 
The period may be much shortened, or much prolonged, or the daily 
step-like fall may be variously disturbed. 

Fever During Convalescence. — This may be (a) that 
of the so-called recrudescence — a transient and sudden rise, attributable 
usually to constipation, to indiscretion in diet or to some excitement; 
(b) that of some complication, and (c) that of a true relapse. 

Relapse s. — These are met with in about 10 per cent, of all cases. 
They are believed to be always a true reinfection by typhoid bacilli 
remaining in the body {e.g., in the gall-bladder). The fever shows 
the same gradual rise and fall as that of the original attack, although 
its course is usually shorter (two to three weeks) . (See Fig. 62.) All the 
other symptoms, including the rose-rash and the enlargement of the 




Fig. 62. — Mild typhoid of 10 days' duration. Temperature normal for one week after this, followed 
by irregular fever as in Chart II. Widal negative, blood culture sterile during this period. Widal posi- 
tive, blood culture positive first time on the 21st day of the disease. 



spleen, are usually seen. The relapse begins in most cases a few days 
(5 to 14) after defervescence is complete, but the internal may be as 
as great as forty or fifty days. On the other hand, it may begin during 
defervescence and before the temperature has reached the normal 
("intercurrent relapse "). A second or even a third relapse is not very 
uncommon. 

These relapses should be carefully distinguished from the other forms 
of post-typhoid fever just mentioned. 

Chills, while not usual in typhoid, are occasionally seen. They 
may mark the onset of the disease or the development of some compli- 
cation. At other times they occur without known cause. 

Pulse. — The pulse is regularly increased in rate, but, in the early 
stage at least, only very moderately. During the first few days it is 
usually below 100 in rate and is full and tense. It soon becomes softer, 
however, and then, frequently, dicrotic. As the disease progresses and 
21 



322 



THE INFECTIOUS DISEASES 



exhaustion increases the rate gradually rises to 120, 130 or even more. 
At the same time the pulse becomes smaller and softer and the dicrotism 
disappears. Irregularity in force or rhythm is not common and is 
apt to be of serious import. During convalescence the pulse rate is 
easily disturbed by slight exertion or excitement. Bradycardia is occa- 
sionally seen at this time. 

Digestive Symptoms. — T o n g u e. — The appearance of the tongue at 
the outset has been described. Later it often becomes a sign of some 
prognostic value. In the mild and moderate cases which are doing well 
it remains moist throughout. In severe cases it becomes very dry and 
tremulous and is often covered by hard, brownish crusts. The gradual 
return of moisture to the tongue is one of the early evidences of 
improvement. 

The appetite is generally lost at the onset and remains so until the 
advent of convalescence. Nausea and vomiting are not common symp- 
toms, but occasionally they may be so persistent and unmanageable as 
to be a serious menace to life. 

Diarrhea is a symptom of much less frequence and importance 
than is popularly supposed. It is present throughout the whole or 
greater part of the attack in rather less than one-third of the cases. 
In another third, approximately, the bowels are constipated throughout, 
or the movements are fairly normal. When present the diarrhea is 
usually not severe and is free from pain and tenesmus. It seems to 
depend rather upon the associated catarrhal enteritis than the specific 
typhoid lesions and bears little or no relation to the severity of these 
latter. Such stools are usually copious, thin, fecal and of light yellow 
or grayish color — the so-called ''pea-soup" stools. Exceptionally the 
diarrhea may be severe and uncontrollable and thus form a conspicuous 
and serious symptom. 

Tympanite s. — A moderate degree of flatulence is commonly 
seen and has little significance. Occasionally, however, the intestinal 
distention becomes very great and persistent and then may cause serious 
disturbance of the cardiac and respiratory functions. It may also 
excite vomiting or persistent hiccough, and it no doubt increases the 
liability to perforation. 

Slight tenderness, especially in the right lower quadrant of the 
abdomen, is frequently met with. Occasionally this may be so marked 
as to suggest appendicitis. Abdominal pain is also sometimes felt, but 
is rarely severe except when due to some complication such as 
perforation. 

The gurgling so frequently felt on pressure in the right iliac fossa 
has little diagnostic value. 

Intestinal liemorrliage and perforation will be discussed under 
complications. 

Eruption. — The characteristic rash of typhoid consists of rose-red 
spots or papules somcAvhat larger than the head of a pin, of velvety 
feel and only slightly elevated. They appear usually about the seventh 



TYPHOID FEVER 



323 



or eighth day of the disease and are scattered sparsely over abdomen, 
chest, back and, less frequently, extremities (see Fig. 63). Occasionally 
they become very numerous over the trunk and extremities, but they 
always remain discrete. Each spot consists of a hyperemic (not hemor- 
rhagic) area which completely disappears upon pressure. They appear 
in successive small crops, each spot persisting from three to five days, 
while the whole eruption lasts from ten to twelve days. In some cases 
the entire eruption will consist of not more than half a dozen spots; 
moreover, the eruption fails altogether in 15 or 20 per cent, of the cases. 
Recently typhoid bacilli have been found in a large portion of the rose 
spots examined and it seems probable that they always contain such 
bacilli. 

Spleen. — Moderate enlargement of the spleen is almost invariable 
and begins early. By the sixth or seventh day its tip can usually be 
felt well below the edge of the ribs. Both palpation and percussion 




J 



Fig. 63. — Typhoid fever with profuse eruption, spots plentiful on abdomen, che.st and arms. 

may, however, fail to discover it if there be much tympanites or abdomi- 
nal rigidity. Slight tenderness is not uncommon. The enlargement 
subsides usually with the abatement of the fever. 

Cerebral Symptoms. — H e a d a c h e, during the first week, is rarely 
altogether lacking. Usually it is a constant dull, frontal or occipital 
pain. Occasionally it takes the form of an intense occipital, temporal 
or facial neuralgia. Sleeplessness, restlessness and mild photophobia are 
common during this period. Occasionally all these symptoms may be 
very marked and to them may be added delirium, rigidity of the neck, 
muscular twitchings, etc., so that the picture may closely simulate that 
of meningitis. 

In the second week the headache and restlessness usually give place 
to drowsiness and mental apathy. The discomforts of the illness are 
less appreciated by the patient, his interest in his surroundinsrs flags 
and he lies most of the time in a drowsy, stuporous condition and shows 
distinct aversion to every sort of mental effort. Delirium is present at 



324 



THE INFECTIOUS DISEASES 



some time in most, but by no means in all, of the cases. Often there 
is merely a slight wandering of the mind at night. The delirium is 
rarely an active, violent one. The possibility that a delirious patient 
may leave his bed, leap from a window or otherwise harm himself must 
always be borne in mind. Usually the patient lies quietly, with open 
eyes and muttering speech, oblivious to his surroundings yet easily 
aroused. As the prostration increases there are added tremor of the 
hands and lips, involuntary twitching of the muscles of the arms and 
legs (subsultus tendinum), and automatic movements of the hands, 
such as picking at the bed clothes. Feces and urine may be passed 
involuntarily or, what is more common, retention of urine may occur 
and require catheterization. 

Blood. — The red cells show a gradual diminution in number and in 
the percentage of hemoglobin, which is usually only moderate and which 
develops chiefly in the latter part of the disease. The condition of the 
leukocytes is of more importance. In contradistinction to most acute 
diseases they are not increased in number. On the contrary, they are, as 
a rule, somewhat diminished; ranging usually between 4,000 and 6,000 
per c.mm. They may, however, at the beginning of the disease, be 
increased to 8,000 or even 12,000-13,000. A pronounced rise in the 
leukocytes sometimes marks the advent of complications. There is also 
a gradual decrease in the relative proportions of the neutrophile poly- 
nuclear cells and an increase in the lymphocytes. 

As has been said, the blood contains the specific typhoid bacilli in 
most, if not in all, cases. 

Urine. — The urine at first is concentrated, scanty and high colored. 
It frequently shows a trace of albumin and a few casts. It may con- 
tain blood, many casts and much albumin, from a complicating nephritis, 
or pus from a pyelitis or cystitis. Typhoid bacilli are found in it in 
about one-fourth of the cases. During the second and third weeks it 
usually, but not always, gives a positive response to Ehrlich's diazo- 
reaction (see Diagnosis). 

Complications. — Digestive Tract. — The two most important com- 
plications are those of intestinal hemorrhage and perforation. 

Hemorrhag e. — True intestinal hemorrhage occurs in from four 
to six per cent, of all cases. It is seen usually in the latter part of the 
second and in the third week, i.e., at the time of the separation of the 
sloughs and the development of the ulcers. Occasionally slight bleeding 
from the congested mucous membrane occurs before the formation of 
the ulcers. The hemorrhage may be so slight as only to tinge a single 
stool or may be so persistent and copious as to prove fatal within a few 
hours. The symptoms of severe hemorrhage are a sudden marked fall 
in temperature, rapid, small pulse, pallor, restlessness, thii^t. even 
syncope. The blood may not be passed until some hours after the symp- 
toms have appeared, but usually appears promptly in the stools. Hemor- 
rhage is always a serious complication; many of the cases are fatal, and 
the danger of further bleeding is always present for many days. Bleed- 



TYPHOID FEVER 



325 



ing from hemorrhoids or fissures in the rectum must not be confused 
with true intestinal hemorrhage. 

Perforation of the intestine is the gravest of the complications 
of typhoid fever. It occurs in from two to five per cent, of all cases 
and is almost always fatal from the septic peritonitis which the escape 
of intestinal contents excites. It occurs directly from extension of the 
typhoid ulcers through the gut and is seen usually during the third and 
fourth weeks of the disease. It may, however, happen in the second 
week or during convalescence. The site of the perforation is usually 
the lowermost part of the ileum, but it occasionally occurs in the colon 
or in the vermiform appendix. It is seen in both severe and mild cases. 
Tympanites, vomiting and coughing are regarded as contributory factors. 

The symptoms of perforation are of the utmost importance, since 
immediate operation furnishes the only hope of recovery. They usually, 
but not always, begin abruptly and characteristically with sudden, 
severe abdominal pain, vomiting, tenderness and muscular rigidity — all 
symptoms of the beginning peritonitis. There is sometimes a temporary 
drop in temperature and a rapid rise in pulse-rate. As the peritonitis 
progresses the fever rises, the abdomen becomes greatly distended, the 
eyes sunken, the features pinched and cold, the breathing rapid and 
shallow and the general condition rapidly worse. The symptoms of 
perforation may be indistinct or lacking in cases in which the typhoid 
symptoms themselves are very severe. A rapid rise in the number of 
leukocytes and the replacement of the normal liver dulness by tympany 
are sometimes valuable aids to the diagnosis of perforation, but in most 
instances the leukocyte change is too slow to be of any value, and the 
liver dulness disappears only in the late stages. 

To be of any avail the diagnosis of perforation must be made at the 
outset, chiefly on the basis of sudden, sharp pain in the abdomen, and 
abdominal rigidity, especially on the right side, and, in the clear-minded 
patient, pain. 

Rarely septic peritonitis has developed without there having been 
actual perforation. 

Suppurative parotitis and acute gastritis are infrequent complica- 
tions. Acute glossitis, ulceration and subsequent stricture of the esoph- 
agus and abscess of the liver are among the rarities. An important 
group of complications are those affecting the gall-bladder and ducts. 
Acute cholecystitis and cholangitis due to infection by the typhoid 
bacilli occur, and gall-stones are a not infrequent sequel to the disease. 
Membranous colitis is a rare complication. 

Circulatory System. — Myocarditis, pericarditis and endocarditis are 
rare, as is also thrombosis of the larger arteries. Acute dilataticm of the 
heart may occur in convalescence. Thromhosis of the large veins, espe- 
cially of the femoral, is much more common and is due to a localized 
phlebitis. This complication is usually not serious, but occasionally 
fragments of such a thrombus have been carried to the lungs and have 
caused fatal pulmonary embolism. 



326 



THE INFECTIOUS DISEASES 



Respiratory System. — A severe acute laryngitis is sometimes met 
with. This ma}^ go on to ulceration and to necrosis of the cartilages. 
Acute hronchitis is very common and occasionally is so severe as to be 
a serious complication. 

Lobar pneumonia occurs rarely as an initial symptom and not infre- 
quently as a complication of the later weeks of the disease. Hypostatic 
congestion of the posterior portion of the lungs is not uncommon as a 
result of the long-continued dorsal decubitus and the enfeeblement of 
the circulation. 

Pleurisy, both serous and purulent, is occasionally seen. 

Urinary System. — Acute nephritis is an occasional complication and 
gives its characteristic symptoms. It occurs both early and late in the 
disease and may be of all grades of severity. Pyelitis and cystitis, due 
to the bacillus typhosus, are sometimes encountered. 

Nervous System. — Neuritis occurs, usually as a late complication, in 
both a localized form and as a multiple neuritis affecting several ex- 
tremities, but chiefly the legs. It is both sensory and motor. The com- 
monest type of localized neuritis is that which causes the exquisitely 
tender toes and feet not infrequently seen in the latter half of the 
disease. Post-typhoid insanity is an infrequent sequel. 

Skin. — Boils and subcutaneous abscesses are very common. Some- 
times profuse sweating is met ^^dth. 

Bed sores develop over the bony prominences — sacrum, elbows, heels, 
etc. — where emaciation is marked, and especially where the skin is irri- 
tated by the involuntary^ discharge of urine and feces. The hair is apt 
to fall out during convalescence, but always returns. 

Miscellaneous Complications. — Otitis media is fairly common. 
Pyemia, arthritis, orchitis and intramuscular hemorrhage are all occa- 
sionally met with. 

Among the commoner sequella^ are to be mentioned periostitis and 
necrosis of the long bones. They develop sometimes months after recov- 
ery, are. chronic in course and frequently contain typhoid bacilli. 

''Typhoid spine" is an obscure spinal affection occurring during 
convalescence and marked by severe pain in the back and other symp- 
toms of vertebral disease, possibly due to periostitis. 

The Association of Typhoid Fever and Malaria. — Typhoid fever, 
developing in one who previously has had malaria and in whom some 
organisms still remain quiescent, will sometimes cause the outbreak of 
fresh malarial paroxysms wuth the appearance of parasites in the periph- 
eral circulation. Such cases are, however, veiy rare. The term "typhoid- 
malaria," so often loosely used, is confusing and misleading and should 
be avoided. 

Diagnosis. — The diagnosis in typical cases is easy and can usually 
be made definitely by the beginning of the second week. The continued 
fever, the relatively slow pulse, the rose spots, the enlarged spleen, 
together with the absence of physical signs suggestive of other trouble, 
are usually conclnsive. In the many variations from the typical course, 



TYPHOID FEVER 



327 



however, the difficulties of diagnosis may be very great and a correct 
judgment can be reached only by a careful weighing of all the symp- 
toms and physical signs. No one symptom can be trusted entirely. 

Laboratory Aids to Diagnosis. — The most useful of these is the 
so-called Widal reaction. This is based on the fact that the blood serum 
of typhoid patients, even if highly diluted, when brought in contact 
with actively motile typhoid bacilli causes prompt cessation of the 
motion of the bacilli and their collection into small groups or clumps. 
The technical details and the limitations of the test cannot here be given. 
A positive reaction is obtained in more than 95 per cent, of all cases 
of typhoid and it is very rarely found in other diseases, so that its pres- 
ence is of very great diagnostic value. Unfortunately it is usually not 
present until the 8th or 10th day and it may not appear until the latter 
part of the disease. 

Cultures. — Typhoid bacilli appear in the blood and in the feces usu- 
ally by the end of the first week and sometimes earlier. Their separation 
from other bacteria in the stools is troublesome, but their detection in 
the blood is sufficiently simple to make it a practical and very valuable 
means of diagnosis in well-appointed hospitals. From 8 to 10 c.c. of 
blood are drawn, under due aseptic precautions, from the median 
basilic vein and inoculated usually in two bouillon flasks. The bacilli, 
if present, appear in from 24 to 48 hours. 

Ehrlich's diazo-reaction in the urine is present in most cases of 
typhoid, but it is occasionally met with also in other febrile conditions, 
such as acute tuberculosis. Its presence, therefore, while strongly sug- 
gestive, is not conclusive of typhoid. The absence of an increase in the 
leukocytes in tj^phoid is often of considerable help in differential diag- 
nosis. The disease is apt to go unrecognized in those cases in which 
the initial symptoms are abnormally severe in certain of the viscera. 
Such cases are often mistaken at first for severe bronchitis, lobar pneu- 
monia, nephritis or meningitis. 

Typhoid fever and malarial fever should not often be confused. Only 
the remittent or estivo-autumnal type of the latter bears a resemblance 
to typhoid. In doubtful cases examination of the blood for malarial 
parasites and for the Widal reaction should clear up the diagnosis. 

Other diseases that may ^be confused with typhoid are, typhus, septi- 
cemia, acute miliary tuberculosis, tuberculous peritonitis, malignant 
endocarditis, influenza, salpingitis and, rarely, appendicitis. 

Prognosis. — The mortality varies greatly in different years and in ' 
different epidemics. In general it ranges between 5 and 20 per cent. 
In recent years it has been much reduced by the improvement in nurs- 
ing and by the introduction of the cold bath treatment. The death rate 
is lowest in children and highest in those of advanced age. It is much 
lower in relapses than in the primary attacks. 

The cause of death in almost half of the fatal cases is the severity of 
the systemic poisoning, as shown by hyperpyrexia, severe nervous symp- 
toms and heart weakness. Next in order of importance are intCvStinal 



328 



THE INFECTIOUS DISEASES 



hemorrhage, perforation and peritonitis, pneumonia and acute nephritis. 

Treatment. — Prophylaxis. — Typhoid fever is a preventable disease. 
The fact that the exciting germs leave the body only through the stools, 
urine and vomited matter and enter the body only through the mouth 
and stomach renders the task of prevention a relatively simple one. 
The responsibility for proper and thorough disinfection in every case 
rests with the physician. The solutions most useful for the disinfection 
of the discharges are (a) carbolic acid (1 to 20), (b) corrosive sublimate 
(1 to 500) and (c) formalin (5 per cent.). The feces and urine should 
be received into vessels containing an abundance of the disinfectant 
solution, should be thoroughly mixed with it and should be allowed to 
stand one hour before being disposed of. Under no circumstances should 
the discharge be thrown into privies, cesspools or upon the ground with- 
out such disinfection. All bedding and linen should be soaked in 
carbolic acid (1-20) for several hours and subsequently thoroughly 
boiled. The buttocks and perineum should be carefully cleaned after 
each defecation with corrosive sublimate solution (1-2000). The hands 
of the nurses, thermometers, bed-pans and everything which may come 
in contact with the discharges should be as carefully disinfected. Dis- 
infection should begin as soon as typhoid fever is suspected and should 
continue well into convalescence. 

Since infection occurs in the great majority of cases by means of 
the drinking water the simple precaution of boiling this thoroughly 
removes all chance of infection through it. If there is reason to fear 
that the milk may be contaminated it should not be used uncooked. 
The same may be said of oysters. Ice from polluted streams should not 
be used. Where open privies and cesspools abound flies may be impor- 
tant carriers of the infection and the greatest care should be exercised 
to prevent them from reaching the articles of food. 

Preventive inoculations have very recently been used in the 
British Army and promise to be of real value. The vaccine consists of 
a broth culture of the bacillus typhosus in which the organisms have 
been killed by heat. 

General Management. — In no disease is careful attention to the 
details of management and nursing so richly rew^arded as in typhoid 
fever. The patient should, even in mild cases, be put to bed at once 
and kept there throughout the disease ; the use of the bed-pan and 
urinal being insisted upon. Whenever possible a single bed with firm, 
even surface should be used, as it greatly increases the patient s comfort 
and facilitates his handling. The room should be quiet, cool and well 
ventilated. The keeping of the bed linen scrupulously clean, free from 
wrinkles and dry, especially when there is incontinence of urine or 
feces, will do much to prevent bed sores. To the same end the patient's 
back should be kept clean and dry, rubbed frequently with alcohol and 
protected by dusting powder or a bland ointment. The mouth should 
be carefully cleansed after each feeding. At the outset the bowels 
should be freel}^ moved by calomel or castor oil. After the first week 



TYPHOID FEVER 



329 



it is wiser to keep them regular by enemata or suppositories. The patient 
is not permitted to leave the bed, except perhaps in very mild cases, 
until the temperature has been normal for at least a week. Water to 
drink should be given at frequent, regular intervals and in large 
quantities. 

Diet. — Food should, in general, be fluid and easily digestible and 
should be given at two-hour intervals, except during the night. In most 
cases milk is the article chiefly to be relied upon. From three pints to 
two quarts per day are usually required. It is frequently better digested 
if diluted with vichy, lime water or plain water, or if partly peptonized. 
Strong meat broths (chicken, mutton, beef), buttermilk, kumyss, egg- 
water, beef juice, thin strained gruels, coffee, and ice-cream may be 
given to vary the feeding. Gelatinous foods, such as calf's-foot jelly, 
have both a theoretical and practical value. Rarely the artificial milk 
foods and ''peptonoids " may be useful. With the beginning of conva- 
lescence the appetite returns and the hunger is often such as to cause 
real suffering. The articles mentioned can be given in larger quantities 
and in greater variety, and to them may be gradually added soft boiled 
eggs, milk toast, junket, custards, scraped meat, bread and butter, toast, 
as the returning appetite and increasing power of digestion call for 
them. Fever is no contra-indication to the giving of solid food, provided 
it be given in small quantities and the patient is able to masticate it 
thoroughly. (See Appendix, p. 592.) 

Medicinal Treatment. — Attempts to find a specific treatment have 
not been successful. No drug is known which has a favorable influence 
upon the typhoid infection itself. Efforts to destroy the bacilli in the 
intestine by the use of salol, /?-naphthol, carbolic acid, etc., have not 
succeeded, and it is quite hopeless to attempt by such means to reach 
the germs which swarm in the intestinal lesions, mesenteric glands, 
spleen and blood. Such drugs may sometimes perhaps be of use, as anti- 
ferment atives, in diminishing meteorism, but even here their usefulness 
is questionable. If intestinal antiseptics are to be used salol (gr. v 
every 3 hours) seems to be the best. The use of antipyretics, stimulants, 
etc., will be spoken of under treatment of the individual symptoms. 

Hydrotherapy. — The treatment of typhoid by cold baths, under the 
leadership of Brandt of Germany, has in recent years done much to 
reduce the mortality and to rob the disease of some of its distressing 
symptoms. Such treatment is in no sense specific. It is doubtful if 
the disease is materially shortened by it. Nevertheless its favorable 
influence upon certain of the symptoms is so evident that it is at present 
in very general use both in this country and in Europe. The reduction 
of the temperature is by no moans the chief effect of such baths. Their 
influence in strengthening the heart action and in improving the serious 
nervous symptoms is even more important. 

Hydrotherapy may be practiced by cohl sponging, wet packs, bod 
baths or tub baths. The first throo methods aro to be recommended only 
in ease the tub baths, for any reason, are impracticable. 



330 



THE INFECTIOUS DISEASES 



Tub Baths. — A portable tub, large enough for the patient to lie at 
full length, is placed near the bed. The patient is lifted to and from 
the bath, which is given whenever the temperature (taken every three 
hours) rises above 102.5° or 103° P. As to the temperature of the bath, 
practice varies greatly, but the very cold baths (60°-65°) are much less 
used than formerly. It is rarely desirable to have the temperature lower 
than 72° and most of the good effects can be obtained by baths of 75° 
or 80°. The patient's comfort is greatly increased by beginning the 
bath at 90° and gradually cooling the water by adding ice. The bath 
should last for 15 minutes and the patient should be vigorously rubbed 
by two attendants throughout that time. During this time also it is 
well to keep the head wet with cold water. It is often desirable to 
precede the bath by the administration of half an ounce of whiskey or 
other stimulant. At the end of the bath the patient is wrapped in a 
dry sheet, covered with a light blanket, given a hot drink and encour- 
aged to sleep. If the baths are being well borne the blueness and shiver- 
ing soon disappear and the patient usually falls into a quiet, restful 
sleep. Intestinal hemorrhage, perforation and severe lobar pneumonia 
are the only positive contra-indications to such baths. Other pulmonary 
complications, such as bronchitis, are often greatly benefited. 

Where tub bathing is not practicable sponge bathing or cold packs 
may be resorted to. They, however, are much less efficient and have 
often proved more unpleasant than the baths above described. 

Treatment of Special Symptoms. — Fever. — The most effective and 
at the same time the safest way of reducing the temperature is by use 
of the cool baths already described. The fall is usually from one to 
three degrees and it is often several hours before the fever reaches its 
former height. In private practice it is often desirable to prescribe some 
mild febrifuge such as the following: Potassii citratis, ovi; spt. 
aetheris nitrosi, giss; aqua, q. s. ad qVi. S. One dessertspoonful in cold 
water every four hours. The use of antipyretic drugs for this purpose 
has, happily, to a considerable extent been abandoned. The continued 
use of such drugs as antipyrine and phenacetin in doses sufficient to 
materially affect the fever is often accompanied by such cardiac depres- 
sion, paUor, cyanosis, etc., as entirely to nullify the good effects of the 
reduction of temperature, and even threaten life. If any antipyretic 
drug is to be used, aspirin or quinine is the least objectionable. 

Diarrhea requires treatment only if the number of movements daily 
exceeds three or four. It may often be corrected by some change in the 
diet. If drugs are required bismuth subnitrate (gr. xx-xxx) or pills 
of acetate of lead (gr. ij) and opium (gr. ss) are usually efficacious. 
When there is tenesmus a starch enema will often give relief. 

Tympanites. — Efforts should be made to prevent tympanites by car;e- 
ful attention to diet. When present nothing, in my experience, is so 
likely to give relief as very hot turpentine stupes to the abdomen 
applied for 15 minutes every hour or two. The frequent passage of a 
long rectal tube is sometimes of great service. The good effects of intes- 



TYPHOID FEVER 



331 



tinal anti-fermentatives (turpentine, salol, charcoal, etc.) may occa- 
sionally be seen, but they are usually disappointing. In severe cases 
cessation of feeding for 12 to 24 hours is helpful. 

Intestinal Hemorrhage. — Treatment is limited chiefly to careful man- 
agement of the patient. He should have absolute quiet and freedom from 
all movement. Food should be stopped altogether for 12 hours or else 
given in very small quantities. Pills of opium, or morphine subcuta- 
neously, should be administered to check intestinal peristalsis. Ice to the 
abdomen is of doubtful value. There is little evidence that the internal 
use of the various astringents and styptics ever does good. Acetate of 
lead and suprarenal extract are commonly recommended, but are 
useless. Bismuth in very large doses may, perhaps, be of service. Sub- 
cutaneous injections of gelatin in the effort to promote coagulation have 
been tried, but have been given up. If the bleeding has been very pro- 
fuse, heat to the body surface, elevation of the foot of the bed, subcu- 
taneous infusion of normal salt solution and vigorous stimulation may 
be required, but these last two measures should not be used unless 
imperatively needed, for fear of exciting further hemorrhage. 

Perforation. — Whenever intestinal perforation is suspected bathing 
should be stopped at once, all food should be temporarily withheld and 
absolute quiet maintained. Early operation offers the only hope of 
relief. About one-fourth of the cases recently operated upon have been 
saved. Since the chances of success are diminished by each hour of 
delay, the importance of prompt diagnosis is manifest. If necessary 
the operation may be done under cocaine. 

Circulatory Failure. — Experimental study has shown that ih ani- 
mals rapidity and weakness of the pulse and evidences of circulatory 
failure developed in the course of bacterial infections result not from 
weakness of the heart but from disturbances in the vasomotor system 
produced by the toxins of the disease. Also against such circulatory 
failure the traditional cardiac stimulants, alcohol, digitalis, and strych- 
nine, have no influence, but camphor, caffeine, applications of cold to 
the splanchnic region, or infusions of normal salt solution have some 
effect. 

These teachings have special application to the circulatory failure 
of typhoid fever. It is undoubtedly true that in most cases of such 
failure the heart can be heard and often felt beating regularly and 
energetically, and yet the pulse is rapid, feeble, perhaps uncountable, 
the body cyanotic, and the patient evidently suffering from circulatory 
failure. Under such circumstances, caffeine, camphor, and the other 
measures mentioned above are indicated. Camphor should be given 
hypodermatically dissolved in olive oil, not in ether, the latter solution 
being much too irritant. One or two grains of camphor may be given 
every 2 hours. 

Caffeine-sodium salicylate or caffeine-sodium benzoate may be used 
hypodermatically in doses of 2 grains or more every 2 or 3 hours. 

Infusions of normal salt solution 300 c.c.-500 c.c, or even 1000 c.c, 



332 



THE INFECTIOUS DISEASES 



may be given and repeated according to indications. An ice-cap or ice- 
coil should be kept applied npon the epigastrium. 

If the heart itself seems to be at fault then digitalis, strychnine, or 
alcohol may be given. The use of alcohol in infectious fevers is the 
source of much discussion. All the experimental evidence is against 
its use ; yet most experienced clinicians still give it, sometimes in large 
quantities. One-half to one ounce of whiskey every three or four hours 
is the ordinary dose. 

Nervous Symptoms. — All the severe symptoms are best relieved by 
cold baths. The early headache and sleeplessness may require phenace- 
tin (gT. v-x), Dover's powder (gr. v-x) or trional (gr. x-xx). 

Recrudescences. — The sudden rises in temperature during convales- 
cence are most commonly due to constipation or to dietetic errors. Fluid 
diet should be at once resumed and, if there is no contra-indication, a 
laxative, preferably castor oil, given. One is often amazed at the 
amount of accumulated feces that such a laxative will bring away, even 
when the diet has been entirely fluid. 

TYPHUS FEVER 
(Spotted Fever. Jail Fever. Typhus Exanthematicus) 

Definition. — This is an acute, highly contagious, infections disease 
marked by an abrupt onset, a febrile course of about two weeks, a char- 
acteristic rash and severe nervous symptoms. 

Etiology. — Predisposing Causes. — Typhus fever is at the present 
day a comparatively rare disease. It occurs endemically in England, 
Ireland, Russia, Hungary and in various parts of Asia and it appears 
in other countries sporadically and in epidemics. A few epidemics have 
occurred in the large seaboard cities of this country. Overcrowding, 
poor food and filth are potent predisposing factors. It is therefore most 
frequently seen in camps and barracks, jails and in the crowded and 
unsanitary portions of large cities. It follows in the path of war and 
famine. Most epidemics occur in the colder months of the year. The 
disease attacks all ages and is seen in males more commonly than in 
females. 

The direct, exciting cause is unknown, but it is doubtless a micro- 
organism of some sort. The disease is one of the most contagious known, 
the contagion being transmitted, as in other such diseases, by the expired 
air, by exhalations from^ the skin, by clothing, bedding, etc. Its con- 
tagiousness is greatest in close, crowded rooms and least in the open 
air and in large, well-ventilated wards. It is probably never trans- 
mitted through food and drink. 

The infectious agent has been proven to exist in the blood of the 
patient, the disease having been transmitted to monkeys in series by 
inoculations of infected blood. The pediculus vestimentorum is re- 
garded as the probable agent by which the disease is conveyed from 
man to man. Predjetschensky has obtained from the blood drawn on 



TYPHUS FEVER 



333 



tJie 6th to the 9th day of the fever a short, thick bacillus, which he 
regards as the causative organism. Sufficient time has not yet elapsed 
to allow proper testing of these plausible propositions. 

Immunity for life is usually provided by one attack. 

Morbid Anatomy. — Aside from the petechial rash w^hich persists 
after death, the lesions found at autopsy are in no wise characteristic. 
They are those of any severe infection — dark fluid blood, parenchyma- 
tous degeneration of heart, liver, kidneys and voluntary muscles, hypo- 
static congestion of lungs, etc. 

Symptoms. — The period of incubation is quite regularly about 
twelve days. It may, however, be as short as one week or as long as 
fifteen days. Prodromal symptoms are usually lacking. 

Onset. — The disease begins abruptly with one or more chiDs, vomit- 
ing, severe headache, backache and pain in the legs. Prostration is 
marked from the outset. The eyes are red and watery and the face 
flushed and swollen. The tongue is dry almost from the beginning and 
is heavily coated. 

Fever. — The temperature rises steadily during the first three or 
four days to 104° or 105° F., or even higher. It then maintains this 
height with only slight daily fluctuations until the latter part of the 
second week (12th to 15th day), when it falls rapidly to normal. This 
period of defervescence usually occupies two or three days. The fall 
may, however, be by crisis. Just before defervescence the temperature 
may be especially high (106° to 107° F.) or there may be a temporary 
fall or pseudo-crisis. 

Eruption. — The rash is one of the characteristic and constant 
features of the disease. It appears quite regularly on the 4th or 5th 
day. It may be accompanied or preceded by a peculiar dusky mottling, 
or a measles-like blotching of the skin, which lasts only a day or two. 
The true rash consists of a single crop of pale, pinkish macules of pin- 
head size or somewhat larger, w^hich at first disappear on pressure. 
These appear over abdomen and chest and rapidly extend to back and 
limbs ; the palms of the hands, soles of the feet and face alone remaining 
free. Within two or three days blood escapes into most of these 
hyperemic areas, they become a deeper red, and no longer disappear on 
pressure. 

The petechial character of the rash constitutes its chief diagnostic 
feature. The spots which do not become petechial disappear in three 
or four days, but the petechias remain for a week or ten days, gradually 
fading to a dirty, brownish stain. Exceptionally the rash is petechial 
from the outset and may be accompanied by subcutaneous hemorrhages 
of some size. The eruption is usually more abundant than that of 
typhoid, which it at first so closely resembles. Moderate enlargement 
of the spleen is usual and occurs as early as the second or third day. 

The PUi.SE is much quickened almost from the beginning, its rate 
being usually between 110 and 120 per minute. At first the pulse is 
full and tense, but in the second week it grows steadily smaller and 



334 



THE INFECTIOUS DISEASES 



weaker and may become almost imperceptible. Dicrotism is much less 
common than in typhoid. The bowels are usually constipated, but diar- 
rhea is not uncommon during the second week. 

The NERVOUS SYMPTOMS are among the most conspicuous of the dis- 
ease. The severe headache of the onset soon gives place to mental 
apathy and this, in many cases, to violent delirium. In the second week 
this delirium merges into deep stupor, with vacant, staring eyes, mut- 
tering speech, wide open mouth and trembling, dry tongue ( coma- vigil ) . 
The patient is entirely oblivious to -his surroundings. Urine and feces 
are passed involuntarily and there are involuntary^ twitchings of the 
muscles of the extremities (subsultus tendinum), and purposeless move- 
ments of the cyanotic, shrunken fingers. In the milder cases there may 
be only apathy and drowsiness with quiet, nocturnal delirium. The 
urine shows no characteristic change. A small quantity of albumin is 
not uncommon. 

In contradistinction to typhoid a distinct increase in the leukocytes 
of the blood is usual, but leukopenia may be found. • 

Variations from the course described are of frequent occurrence. 
]\Iild cases of short duration are frequently seen, especially toward the 
end of an epidemic. Malignant cases, fatal within a few days, are met 
with. Earely, too, cases of three weeks' duration are encountered. 

Convalescence. — With the critical fall of temperature there is a 
correspondingly rapid improvement in the other symptoms. The skin 
is bathed with profuse perspiration. The stupor and delirium give 
place to a refreshing sleep, the pulse becomes slower and stronger. 
Relapses are extremely rare and later complications not very common, 
so that the convalescent patient usually progresses steadily and fairly 
rapidly to recovery. 

Complications and Sequelae. — Pulmonars^ complications are the 
most important and include severe bronchitis, bronchopneumonia, hypo- 
static congestion and gangrene; otitis media, laryngitis, gangrene of 
the extremities, venous thrombosis, nephritis, peripheral neuritis and 
hemiplegia, and subcutaneous abscesses also occur. 

Diagnosis. — The disease during its early stages is often extremely 
difficult to diagnosticate. Small-pox, scarlet fever, measles, meningitis 
and typhoid fever all may be confused with it. A careful study of all 
the symptoms, and especially of the fever and the nature of the eruption, 
is needed to clear away the doubt. From typhoid fever the disease is 
differentiated by its more rapid and violent onset, the swollen face and 
suffused eyes, the increase in leukocytes if present, the absence of the 
Widal reaction, negative blood cultiuTs, and especially by time of ap- 
pearance, distribution and character of the eruption. This appears 
earlier, is more abundant on the arms and legs, does not come out in 
successive crops, is less distinctly elevated and, in the course of two or 
three days, becomes petechial, at least in part, and then no .longer dis- 
appears upon pressure. In fatal eases the absence of the post-mortem 
lesions characteristic of typhoid fever is most important. 



EELAPSING FEVER 



335 



Prognosis. — The mortality varies greatly in the different epidemics. 
In general it may be said to amount to 15 or 20 per cent. In single 
epidemics it may reach 50 per cent. The death rate is lowest in chil- 
dren and highest among the debilitated, the alcoholic and aged. 

Treatment. — The highly contagious nature of the disease demands 
the most careful isolation and disinfection. Free ventilation is known 
to diminish greatly the chance of contagion for those in attendance as 
well as to be beneficial to the patient himself. No specific treatment is 
known. The use of drugs should be limited to the treatment of such 
special symptoms as heart weakness, cough, etc. For the fever and the 
severe nervous symptoms hydrotherapy (preferably by tub baths) is the 
most rational treatment. This, as well as the dietetic treatment, should 
be carried out along the lines suggested for typhoid fever. 

RELAPSING FEVER 
(Recurring Fever. Famine Fever. Seven-day Fever) 

Definition. — An acute infectious disease caused by a specific micro- 
organism, the spirillum of Obermeier ; and marked by two or more severe 
febrile attacks, each of several days' duration, w^hich are separated by 
afebrile intervals of similar length. 

Etiology. — The disease at the present day is rare. Epidemics ap- 
pear from time to time in various parts of Europe and in the British 
Isles. It is said to be common in India. A few epidemics have occurred 
in New York and Philadelphia — the last one in 1869. 

In its PREDISPOSING CAUSES it is closely allied to typhus fever in that 
filth, overcrowding and famine are the conditions which chiefly favor 
its development. Age, sex, and season seem to have little influence. 

The EXCITING CAUSE is a blood parasite, a spirillum or spirochete, 
which was first seen by Obermeier in 1873. It is a slender, actively motile, 
spiral filament whose length is several times the diameter of a red cell. 
These germs are constantly present in the blood plasma during the 
febrile paroxysm, but disappear just before the crisis and are not to be 
seen during the intervals. They have not been found in the body secre- 
tions or elsewhere than in the blood. Little is known of their life his- 
tory. The disease has been transmitted to man and monkeys by the 
inoculation of infected blood. It is believed to be contagious by direct 
transmission and by means of fomites, but in the light of our present 
knowledge of the mode of transmission of malaria and yellow fever it 
seems possible that direct inoculation into the blood, by insects or other 
means, may be found to be necessary. 

Morbid Anatomy. — No characteristic lesions are found after death. 
There are parenchymatous degeneration of the viscera, swelling of the 
spleen and sometimes jaundice. 

Symptoms. — The incubation period commonly lasts from five to 
seven days. It may, however, be considerably shorter or longer. 

The ONSET is sudden, with a distinct rigor and an immediate rise of 



336 



THE INFECTIOUS DISEASES 



temperature. There are also pains in the head, back and limbs; vomit- 
ing and prostration. Within a few hours the fever rises to 104° or 
105° F., and then remains constantly high (104° to 107° F.) for several 
days. Sweating, cough, delirium and jaundice may be present. The 
pulse is rapid and' full ; the spleen becomes enlarged early and the blood 
shows an increase in leukocytes. Herpes labialis is sometimes seen. 
In severe cases cutaneous petechige and ecchymoses may occur. (See 
Fig. 64.) 

On the 6th or 7th day, usually, the paroxysm ends by crisis. With 
the sudden fall of temperature to normal or below there is profuse 
sweating and sometimes diarrhea. In debilitated subjects the collapse 
may be profound. The temperature remains normal in most cases for 
about a week and there is a corresponding remission in all the other 
symptoms; then the patient again has a chill (or several chills) and 
a rise of temperature, and the first attack is repeated except that the 
duration is apt to be somcAvhat shortened. After a second crisis mid 
afebrile period a third, and even a fourth and fifth paroxj^sm may occur. 




Fig. 64. — Temperature of relapsing fever, showing the conclusion of one paroxysm. The afebrile period, 

and a new paroxysm. 

Variations from the above typical course are frequent as regards 
the duration of both the febrile attacks and the free intervals. In some 
mild cases no relapse occurs. In severe cases jaundice may be a con- 
spicuous feature. 

Complications. — There may be pneumonia, nephritis, neuritis, 
ophthalmia, hemorrhage of stomach, intestines or kidney, or rupture of 
the enlarged spleen. 

The PROGNOSIS is usually good. The death rate is low (4 per cent.), 
but varies much in the different epidemics. 

Diagnosis. — In its onset relapsing fever cannot be distinguished 
from a number of other infectious diseases. Its later coursCj however, 
is so characteristic that it can hardly be misinterpreted and a positive 
and easy means of diagnosis is at hand in the examination of the blood. 

The parasites disappear from the blood in the afebrile stage, but 
Lowenthal has shoA\Ti that if a drop of blood from a patient in this 



INFLUENZA 



337 



stage be mixed with a drop from another patient in the febrile stage and 
therefore containing the spiroehetae, the preparation sealed and placed 
in a thermostat for one-half hour, the organisms lose their motion. In this 
manner mild or abortive types of the fever may also be recognized. 

Treatment. — Drugs seem to have no effect upon the course of the 
disease. The cases must be treated symptomatically along the lines 
suggested under typhoid fever. Isolation and disinfection should be 
rigidly enforced. Injections of arsenobenzol, 0.3-0.5 gm., as for syphilis 
(see p. 450), are said to be effective. 

INFLUENZA 
(La Grippe) 

Definition. — An acute febrile epidemic disease, due to a specific 
micro-organism, and characterized usually by catarrhal symptoms, by 
great prostration, by inflammation of the various mucous membranes, 
especially of those of the respiratory tract. 

Etiology. — The disease has for centuries occurred in vast epidemics 
which, beginning usually in Russia, have spread rapidly over the greater 
part of the world. For several years after such an epidemic many 
sporadic cases are seen, especially in the colder months of the year. 
The disease attacks all ages and both sexes indiscriminately. The direct 
exciting cause is the hacillus influenzce, a very small, non-motile 
organism discovered by Pfeiffer in 1892, found abundantly in the secre- 
tions from the inflamed membrane. 

Morbid Anatomy. — Aside from a catarrhal inflammation of the 
affected mucous membranes no lesions are found post mortem except 
those of the various complications. 

Symptoms. — The period of incubation is iLsually from two to four 
days. The onset is quite abrupt, with a sudden rise of temperature 
to 103° or 104° F., chilliness, headache, severe pain in the back and limbs 
and, usually, great prostration. (See Fig. 65.) According to the pre- 
dominance of special symptoms the cases are divided into the catarrhaij 
TYPE, with symptoms of coryza, laryngitis or bronchitis; the nervous 
TYPE, in which the chief symptoms are severe headache, insomnia, neu- 
ralgia, and pain in the joints; the gastro-intestinal type, with per- 
sistent nausea and vomiting or severe diarrhea, and the febrile type, in 
which high fever is almost the only symptom. 

Course. — In uncomplicated cases most of the symptoms subside in 
from three to seven days, although the prostration which is often so 
prominent a feature may persist much longer. 

Complications. — The disease is marked by a tendency to the develop- 
ment of a great variety of serious complications, of which pneumonia is 
much the most important. Influenzal pneumonia, although similar to 
lobar pneumonia in its histological features, differs from the latter 
clinically in its association with extensive bronchitis, its tendency to 
develop irregular areas of consolidation in both lungs, its frequent 
defervescence by lysis, and its higher mortality. Severe bronchitis fre- 
22 



338 



THE INFECTIOUS DISEASES 



quently occurs without evident pneumonia. Other occasional complica^ 
tions are otitis media, pleurisy, endocarditis, pericarditis, cardiac irreg^ 
ularity of obscure nature, venous thrombosis, nephritis, meningitis, 
neuritis, melancholia, etc., etc. 

Diagnosis. — Great caution should be exercised in the diagnosis when 
no epidemic prevails. The sudden violent onset, severe pains and pros- 
tration are the features most to be relied upon. The term ''grippe" 
is loosely and improperly applied to many cases of simple coryza, ton- 
sillitis, bronchitis, etc., which bear no relation to true influenza. 

The only satisfactory basis for the diagnosis of influenza is the 
demonstration of the Pfeiffer bacillus in large numbers in the sputum, 
or other secretion, such as the cerebrospinal fluid. On this basis influ- 
enza is now a rare infection. The great majority of cases to which the 
name is ordinarily applied are infections by other organisms, such as 
the staphylococci, streptococci, the micrococcus catarrhalis, etc. 




Fig. 65. — The irregular fever of influenza. 

Prognosis. — The prognosis of true influenza varies with the age 
and general condition. During epidemics the disease proves very fatal, 
especially through the complicating pneumonia. The weak and debili- 
tated, especially elderly people, frequently succumb. In the young and 
vigorous influenza is rarely fatal, but protracted anemia and debility 
often follow. 

Treatment. — The patient should immediately be put to bed and 
upon a fluid diet, and a brisk purge given. The fever and the pains 
are usually best combated by the combination of an antipyretic and 
a salicylic compound, e.g., phenacetin and salol, or aspirin 5 grains 
every three or four hours. If cardiac depression be marked, stimula- 
tion by strychnine, caffeine or alcohol may be needed. When gastric 
symptoms are prominent, it is often necessary to Avithhold all medication 
for a time and to give fluid food only in minute and frequently repeated 
doses.'' Removal to a milder climate and rest are often necessary to 
convalescence. 



YELLOW FEVER 



339 



DENGUE 

(Break-Bone Fever) 

An epidemic, infectious disease of warm climates marked by one or 
more paroxysms of fever, intense pains in the bones and joints and a 
skin eruption. 

Etiology. — Epidemics of dengue have been seen in various tropical 
and sub-tropical countries, and a number have occurred in the Gulf 
States of this country. The disease resembles influenza in its rapid 
spread and in the fact that it attacks a large proportion of the popula- 
tion of all ages. Evidence is accumulating to show that the mosquito is 
the chief means of transmission, and a parasite similar to the Plas- 
modium of malaria has recently been found in the blood cells. The 
disease usually appears during the warm months of the year. 

Nothing is known of its morbid anatomy, since it is rarely fatal. 

Symptoms. — The incubation period is from two to five days. The 
onset is very sudden, w4th intense pains in the joints and bones, head- 
ache, and a rapid rise of temperature to 104° or 105° F. or even higher. 
The pulse is proportionately rapid, the tongue coated, the face flushed 
and swollen, the urine scanty and the bowels constipated. A transient 
erythematous rash is often seen at the beginning of the disease. The 
pains attack many of the joints, which are usually also tender and 
swollen. At the end of three or four days there is a marked remission 
for two or three days of the temperature and the agonizing pains, 
after which the fever and pains return for two or three days and there 
is usually also an eruption, which may be measly, scarlatiniform or urti- 
carial in character. At the same time there is often enlargement of 
the lymph glands. Hemorrhages from the mucous membranes occur 
rarely. The disease usually lasts from seven to ten days, although pros- 
tration, pains and stiffness may persist for some time longerr. The prog- 
nosis is perfectly good, fatal cases being almost unknown. Complica- 
tions are rare. One attack does not afford complete immunity. 

Diagnosis. — The epidemic character, the prominence of the joint 
symptoms and the late eruption are the features of special diagnostic 
value. The disease may be confused with influenza, acute articular 
rheumatism, epidemic meningitis or yellow fever. 

Treatment. — The diet should be fluid. Morphine hypodermically 
is often needed to relieve the excruciating pains. Antipyrine or phe- 
nacetin may suffice in the less severe cases. Very high temperature or 
delirium demands cold sponging or packs. If prostration is marked 
stimulation by alcohol or strychnine may be needed. 

YELLOW FEVER 

Definition. — Yellow fever is an acute, non-contagious, infectious dis- 
ease marked by a sharp febrile paroxysm, albuminuria, jaundice and a 
tendency to hemorrhage, especially into the stomach. It is transmitted 
by the bite of certain infected mosquitoes. 



340 



THE INFECTIOUS DISEASES 



Etiology. — The disease is endemic only in a few well-defined trop- 
ical districts, which include certain of the sea-ports of the West Indies, 
of Central America and of tropical South America, and certain parts 
of the coast of West Africa. From these foci it occasionally spreads in 
large epidemics to temperate regions and especially to the southern 
portion of the United States. It is rarely seen at altitudes of above 1000 
feet and epidemics are usually promptly checked by frost. Yellow fever 
attacks both sexes and all ages, but is usually seen in young adults. The 
negro race is relatively immune. Its transmission has been definitely 
proven to be by means of infected mosquitoes of the species Stegomyia 
fasciata, and not, as has always been supposed, by mere personal con- 
tact or by infected fomites (see Fig. 66). 

The germ of yellow fever is unknown. However, the Yellow Fever 
Commission of the United States Marine Hospital Service has offered 
much evidence to show that it may be an animal parasite, closely related 
to the malarial Plasmodium, which finds its intermediary host in the 
mosquito above mentioned. 

Morbid Anatomy. — The post-mortem findings include deep jaun- 
dice of the skin and tissues generally, petechial and larger hemorrhages 
into the skin, muscles and serous and mucous membranes, and acute 
parenchymatous degeneration of the liver, kidneys, and heart. The 
liver especially shows marked changes. It is usually small and of a 
pale brownish color and reveals extensive fatty degeneration of its cells 
with areas of focal necrosis. The diagnosis of yellow fever cannot safely 
be made from the autopsy findings alone. 

Symptoms. — The period of incubation lasts from one to five days. 
The symptoms are usually divided into three periods. 

(1) Stage of Invasion, or Febrile Stage. — The onset is abrupt and 
is marked by a distinct chill. The fever rises rapidly to 103° or 104° F., 
the pulse is rapid and bounding, there are headache, pain in back and 
limbs, nausea, vomiting and a hot, dry skin. The face has a peculiar 
swollen, flushed look, the eyes are injected and the sclerotics, even on 
the first or second day, usually reveal the beginning jaundice. The 
tongue at first is coated and moist, but soon becomes dry and brown. 
Vomiting usually persists and may even in this stage become hemor- 
rhagic ("black vomit"). The urine is scanty and within a day or two 
becomes albuminous. The fever continues high, the pulse grows weaker 
but at the same time becomes slower. Jaundice may be slight or well 
marked. Distinct enlargement of the spleen is uncommon. This stage 
lasts from one to four days and is followed by 

(2) Stage of Calm. — The fever rapidly falls to about normal, the 
vomiting ceases, the jaundice lessens and the patient is much more 
comfortable. This may mark the beginning of convalescence, but in 
many cases, after some hours or a day or two, the symptoms all return. 

(3) Stage of Reaction. — The fever again becomes high and all the 
constitutional symptoms return. Jaundice deepens, hemorrhages occur 
beneath the skin and from the various mucous membranes, especially 



YELLOW FEVER 



341 



into the stomach, whence the blood is vomited in the form of brownish, 
grumous material which constitutes the dreaded "black vomit." The 
patient becomes delirious, the urine is often altogether suppressed, the 




pulse is small and very feeble, but is often strikingly slow (60 to 80). 
Most of the cases which enter this stage die within one or two days. In 
the few that recover convalescence is apt to be slow and tedious. One 
attack usually confers immunity for life. 



342 



THE INFECTIOUS DISEASES 



Diagnosis. — The features upon which the diagnosis is to be based 
are the violent onset, the characteristic facies, the early albuminuria 
and jaundice and the falling pulse rate with a high or rising tempera- 
ture. The disease may readily be confused with the severer form of 
malarial fever, in which, however, the jaundice and albuminuria are 
less common and appear later, the spleen is much enlarged and the blood 
contains the malarial Plasmodium. Dengue also may occasionally give 
a clinical picture closely resembling that of yellow fever. 

Prognosis. — The mortality varies in different epidemics between 10 
and 75 per cent. A very high temperature, suppression of urine and 
the black vomit are especially grave symptoms. 

Prophylaxis. — The modern view that yellow fever is not contagious 
and is spread only by the bites of infected mosquitoes seems to show 
that the rigid quarantine hitherto in vogue is unnecessary. Rational 
prophylaxis lies in preventing those sick of the disease from being bitten 
by mosquitoes and in protecting healthy persons from the bites of any 
mosquitoes which may possibly be infected, and in destroying the mos- 
quito so far as possible. The success of the United States authorities 
in checking the outbreak of 1905 in New Orleans by these measures and 
the prevention of outbreaks in Panama have thoroughly established the 
correctness of this theory. 

Treatment. — This is purely sj^mptomatic. An active purge should 
be given at the onset; the fever is to be combated by bathing or by 
cold packs and the heart supported by strychnine, digitalis and alcohol. 
Great care should be exercised in the feeding and in the administration 
of drugs to avoid irritation of the stomach. Only fluid foods such as 
broths or milk and vichy should be given and these only in small quanti- 
ties. If vomiting is severe it may be necessary to ^^dthhold for two or 
three days all food and drink by mouth and to supply nourisliment only 
by the rectum. For the tendency to hemorrhage little can be done. 
Calcium chloride by mouth or rectum and subcutaneous injections of 
gelatin may be tried. 

Sternberg's plan of treatment has been generally approved. Sodium 
bicarbonate 2i/2 drams and bichloride of mercury gr. Ys are dissolved 
in 1 quart of water: of this solution an ounce and a half is given every 
hour. 

THE PLAGUE 
(Bubonic Plague. Pest) 

Definition. — An epidemic infectious disease of great fatality, due to 
the invasion of a specific bacterium — Bacillus pestis — and marked clin- 
ically by severe constitutional symptoms and the development usually 
of suppurative buboes. 

Etiology. — Bubonic plague, the ''Black Death" of the Middle Ages, 
has been kno^^^l as one of the great pestilences for many centuries. In 
London in 1665 it destroyed 70,000 lives, or more than one-seventh of 
the total population. The last great epidemic began in China in 1894 



THE PLAGUE 



343 



and for several years raged with great virulence througliout India. A 
number of cases appeared in San Francisco in 1890. In 1910 and 1911 
the disease ravaged Manchuria and Northern China. It seems to be 
endemic in certain parts of Asia and in Uganda. Age, sex, and occu- 
pation have little influence upon susceptibility. It prevails chiefly in 
the hot months. Filth and overcrowding are the factors chiefly influ- 
ential in determining its spread. It is therefore confined almost exclu- 
sively to the native population. Doctors, nurses and those living under 
proper hygienic conditions are rarely attacked. Infection probably 
occurs through both the digestive and the respiratory tracts and also 
through abrasions of the skin. Rats and mice are very susceptible to 
infection and are believed to play an important role in the spread of the 
disease. There is now much evidence that the bites of the rat-flea may 
be the chief means of infection. In Manchuria the disease was believed 
to be spread by the infected skins of the marmot. The ground-squirrels 
of California have been shown to be widely infected. The infection is 
probably conveyed through foods (such as rice) and water. 

Bacillus pestis, discovered by Kitasato and Yersin in 1894, is a very 
short, thick rod with rounded ends, and is found abundantly in the 
inflamed lymph-nodes and in the blood, viscera, and the various 
excretions. 

Morbid Anatomy. — The post-mortem appearances are very similar 
to those of other severe infections. The blood is dark and fluid ; hemor- 
rhagic extravasations are seen in the serous and mucous membranes; 
the liver and spleen are swollen ; there is parenchymatous degeneration 
of the various viscera. Many of the lymph-nodes are inflamed and some 
of these show foci of suppuration. Hypostatic pneumonia is common. 

Symptoms. — The incubation period is usuall}^ less than one week; 
most commonly from three to five days. The onset is sudden, usually 
without prodromata, and consists of headache, malaise, fever and great 
muscular weakness. A rigor is not common. 

The disease appears in four forms. Of these the ordinary or severe 
type {pestis major) is marked by high fever (104°-105° F.), great pros- 
tration, anxious look, rapid pulse, dry, brown tongue, and, after three 
days, by the appearance of glandular swellings (buboes) which may 
reach the size of an egg and which usually suppurate and break down. 
These buboes are present in about three-fourths of the cases and most 
frequently occur in the inguinal glands. Less commonly they develop 
in the axillary or cervical glands. A tendency to hemorrhage from the 
mucous membranes and into the skin is common in the later days of 
the disease. 

(2) The mild form, (pestis minor) is seen chiefly at the beginning of 
an epidemic and is characterized by symptoms of only moderate severity 
and by the absence of glandular swellings. 

(3) The malignant type {pestis siderans) is marked by symptoms 
of an intense septicemia which is usually fatal within a day or two 
and before buboes have had time to develop. 



3U 



THE INFECTIOUS DISEASES 



(-1) The pneumonic type presents the symptoms and signs of severe 
pneimionia. The recent ]\Ianchiirian outbreak was wholly pneumonic in 
type and invariably fatal. 

Prognosis. — The mortality ranges between 50 and 90 per cent. The 
malignant and pneumonic cases are almost uniformly fatal, as are also 
many of the cases of the common bubonic type. 

Diagnosis. — Cultures from the local lesions or from the blood regu- 
larly yield the characteristic organism. 

Treatment. — Prophylaxis demands careful isolation and the disin- 
fection of all discharges, clothing, infected houses, etc. Special atten- 
tion should be paid to the destruction of rats and to the protection of 
exposed persons from the bites of fleas and other insects. As the pneu- 
monic type is probably conveyed from one pei^on to another by inhala- 
tion, phj^sicians and other Avorkers in the ]\Ianchurian epidemics were 
protected by a respirator consisting of antiseptic cotton between layers 
of gauze, as well as a head dress, overalls, and rubber gloves. 

Serum Treatment. — Hafflvine's preventive serum seems to confer 
a fair amount of immunity for a few weeks and to mitigate the severity 
of the symptoms in those attacked. The value of Yersin's curative 
serum seems not yet to be fully established. 

Lustig and Galeotti dissolve agar-agar plate cultures of the bacillus 
in 1 per cent, caustic potash solution, precipitate the nucleoproteids by 
the addition of weak acetic or hydrochloric acid, wash and dry the 
precipitate in vacuo. Three milligrammes of this substance dissolved in 
0.5 per cent, carbonate of soda are given by injection. A marked local 
and general reaction follows the inoculation, the reaction becoming less 
with each repetition of the injection. Favorable results have been 
reported from the use of these inoculations in man. By treating the 
horse with these injections a serum which is both protective and curative 
in animals has been obtained. Othen^ise the treatment of the disease 
is purely symptomatic. 

MALTA FEVER 
(Undulant Fever. Mediterranean Fever) 

Definition. — ]\Ialta fever is a specific infectious disease of protracted 
febrile course endemic in Malta, Gibraltar and the regions bordering 
on the Mediterranean. A few cases have been met Adth in other 
parts of the world. It attacks young adults chiefly and is most 
prevalent in summer. The specific agent is the Micrococcus mclitensis 
(Bruce), which is found abundantly in the spleen and lymph-nodes 
and rarely in the blood. The disease is not contagious. The fever is 
spread in ]\Ialta through the common use of goat s milk. Fifty per cent, 
of the goats on the island are infected. 

Morbid Anatomy. — Fatal cases show no characteristic lesions. The 
spleen is much enlarged and soft and there is sometimes a complicating 
pneumonia. The organism can be cultivated from the spleen and lymph- 
nodes. 



BERI-BERI 



345 



Symptoms. — The onset is slow and resembles closely that of typhoid 
fever. The disease runs a very protracted course of from two to six 
(or more) months, made up of a series of febrile Avaves, each lasting 
from one to three weeks. The fever rises and subsides gradually and 
the waves are separated by a few days' interval of normal or nearly 
normal temperature. In some cases these undulations are not present 
and there is a continued fever with daily remissions or intermissions. 
Gradual emaciation, weakness and anemia follow, but delirium and 
severe toxic symptoms are rare. Constipation, profuse sweating and 
neuralgic pains are common. Almost the only physical sign is the 
constant great enlargement of the spleen. 

Inflammations of the joints and testicles are frequent complications. 

Diagnosis. — From typhoid the disease may be distinguished by the 
peculiar course of the temperature and by the absence of an eruption, 
of diarrhea and of the AA^idal reaction and by the results of blood cul- 
tures. Moreover, the blood-serum, even when highly diluted, causes the 
prompt agglutinization of cultures of the micrococcus melitensis, and 
this organism can be isolated from the splenic blood obtained by 
puncture. 

Prognosis. — Almost all the cases recover in spite of the greatly 
prolonged and tedious course, the mortality being only 2 per cent. The 
rare fatal cases usually run a short course with very high fever and 
severe toxic symptoms. 

Treatment. — The treatment is purely symptomatic. 

BERI-BERI 

Definition. — Beri-beri is an endemic and epidemic disease of warm 
countries, probably infectious in nature, characterized by a neuritis 
affecting chiefly the peripheral, cardiac and vasomotor nerves. 

Etiology. — The disease prevails in many tropical and sub-tropical 
regions, especially in Japan, China, the East Indies and South America. 
A few epidemics have occurred in asylums in our Southern States and 
cases have been met with among the Gloucester fishermen. It exists 
endemically in many regions and from these may spread from time to 
time in the form of epidemics. It attacks chiefly the native population 
and is prone to appear in crowded, damp and unsanitary ships, asylums, 
barracks, etc. It is favored by hot, damp weather. Young adult males 
are those most frequently attacked. 

Two theories are held concerning its causation. The one more gen- 
erally accepted is that it is a specific infectious disease. The other view 
regards the disease as a species of toxemia due to the eating of certain 
kinds of food, especially of diseased rice or of raw fish. No germ has 
yet been proven to be the exciting cause. The disease is not directly 
contagious. 

Morbid Anatomy. — The characteristic lesion is that of a neuritis 
with degeneration of the nerve fibers and of the associated muscles. 



346 



THE INFECTIOUS DISEASES 



When the vagus is involved the heart is frequently much dilated and 
shows parenchymatous degeneration. 

Symptoms. — These vary much both in character and in severity. 
When the nerves of the extremities are chiefly affected the clinical 
picture is very similar to that of alcoholic neuritis. When, as often 
happens, the cardiac and vasomotor nerves are involved cardiac dis- 
turbance, dj^spnea and anasarca are the conspicuous symptoms. Four 
clinical types may be recognized: 

(1) A mild or rudimentarj^ form in which, with or without vague 
prodromal symptoms, there appear weakness and pains in the legs, 
tenderness of the calf muscles, dulling of tactile sensation or pares- 
thesia of the arms and legs, slight edema and some breathlessness and 
cardiac irritabihty. These sATQptoms may last for weeks or months. 

(2) The Atrophic or Dry Form. — In this there are marked loss of 
power in the arms and legs, much wasting of the muscles, loss of the 
deep reflexes, tenderness of the muscles, pain, and anesthesia or hyper- 
esthesia of the skin. Cardiac symptoms and dropsy are usually slight 
or lacking, but death sometimes occurs from sudden heart failure. ]\Iost 
cases recover after many months of illness. 

(3) The Dropsical or Wet Form. — Dropsy is a conspicuous feature. 
There are marked edema of the subcutaneous tissue and effusion into 
the serous ca\dties. The heart action is weak and often irregular and 
there is much dyspnea. The evidences of peripheral neuritis are rela- 
tively slight. 

(4) The Acute, Pernicious Form. — This is a very fatal type which 
may run its course in a day or two, but which usually lasts for several 
weeks. There are grave disturbance of the heart action and great dys- 
pnea, which may be constant, but is apt to appear in paroxysms of 
alarming severity. Involvement of the phrenic nerve may cause 
paralj^sis of the diaphragm. The heart is usually much dilated. Death 
usually results suddenly from cardiac failure. 

Prognosis. — The mortality varies in different epidemics from three 
to fifty per cent. The prognosis is always uncertain, since even in the 
apparently mild cases sudden death may result from vagus neuritis. 

Treatment. — Whenever possible the patient should be at once re- 
moved from the infected region and placed under the best hygienic 
conditions. An abundance of nitrogenous food is required and rice 
should be avoided. Absolute rest in bed and cardiac stimulants are 
demanded if the heart symptoms are pronounced. For the paralyzed 
muscles galvanism and massage are often of value. 

SCARLET FEVER 
(Scarlatina) 

Definition. — Scarlet fever is an acute, contagious disease character- 
ized by an abrupt onset, fever, sore throat, and a diffuse erythematous 
rash. 



SCARLET FEVER 



347 



Etiology. — The disease is one of the common exanthemata of child- 
hood and is found scattered widely over the whole world. It is 
endemic in most cities, and in less thickly populated districts occurs 
sporadically and in small or moderate sized epidemics. It attacks 
chiefly children between the ages of tAvo and ten years and is rare in 
infancy and in adult life. The sexes are equally susceptible. Most 
of the cases occur in the colder months of the year. 

Scarlet fever is only moderately contagious. Not more than half 
of the children exposed to the disease contract it. It is contagious from 
the onset of symptoms to the end of desquamation. Of recent years less 
importance has been given desquamation and more emphasis put upon 
discharges from the throat, nose, or ears. The contagium is given off 
from the skin, in the discharges from the nose, throat and ear, and 
probably in the urine and feces. The disease is transmitted by direct 
contact; by means of a third person (nurse, physician, etc.), or by 
fomites (clothing, toys, carpets, etc.). The poison is notably resistant 
and may remain active in a room, or in clothing, for months or even 
for a year or more. Recently a few epidemics have been traced to con- 
taminated milk. 

The germ of scarlet fever is still unknown. The streptococcus pyog- 
enes is the bacterium usually found in the severe throat and ear 
complications. 

One attack almost always confers immunity for life. 

Morbid Anatomy. — The only essential lesions are those of the skin 
and throat. There is a severe acute dermatitis, as shown by intense 
hyperemia, exudation of round cells and edematous swelling, which 
results in the death of the epidermis and its desquamation. In the 
throat there is usually a severe catarrhal pharyngitis. The other lesions 
found at autopsy will be mentioned under Complications. 

Symptoms. — The incubation period is regularly less than one week. 
Most commonly it is three or four days. It may, however, be less than 
24 hours. 

Invasion. — The onset is almost always sudden, with vomiting, pros- 
tration, sore throat and fever. In young children a convulsion is not 
uncommon. The temperature rises rapidly and is directly proportionate 
to the severity of the case. In severe cases it may reach 104°-105° F. by 
the end of the first day. The skin is dry and hot, the pulse very rapid, 
the tongue coated and the pharynx and fauces usually show a diffuse 
reddening. 

Eruption. — Between 12 and 36 hours after the first symptoms 
there appears upon the neck and chest a rash composed of minute, red, 
punctate spots which rapidly spreads over trunk, extremities and face 
and becomes an intense, diffuse scarlet flush. The lips and chin usually 
escape and show a pallor in striking contrast to the appearance of the. 
rest of the body. In mild cases the eruption may be faint and may not 
be seen at all upon the face. Occasionally, too, it is not uniform and 
diffuse, but occurs in large blotches or in macular spots resembling 



348 



THE INFECTIOUS DISEASES 



measles. The rash remains distinct for two or three days and then 
gradually fades, the whole duration being from three to seven days. 
(See Fig. 67.) 

While the rash is distinct the fever remains high and there is much 
burning and itching of the inflamed skin. The child may be either 
very restless or stuporous. Often there is active delirium. The severity 
of the throat symptoms varies greatly. Usually there are redness and 
swelling of the pharynx, tonsils, fauces and uvula, with some pain 
on swallowing and some swelling and tenderness of the submaxillary 
lymph-nodes. The tongue at first is coated with a white fur, but later is 
dry and red. The papilla are swollen and project above the surface of 
the dorsum, producing the so-called ''strawberry tongue." With the 
fading of the eruption the temperature gradually falls and the other 
constitutional symptoms subside. The duration of the fever is com- 
monly from seven to ten days. 




PDLSE 
tLi. 



Fig. 67. — Temperature curve of uncomplicated scarlet fever. 

Desquamation. — As soon as the rash disappears there begins a 
desquamation or ''peeling" of the dead epidermis, which is first noticed 
upon the chest and neck and extends to all parts of the body where 
the rash has been pronounced. Over the trunk it occurs in flakes and 
scales, but on the hands and feet, where it is always marked, the epi- 
dermis comes off in large strips or even as whole casts of the fingers or 
toes. This form of peeling is very characteristic of the disease (see 
Figs. 68, A and B). 

The period of desquamation lasts from two to four, or even to six, 
weeks. The process is slowest on the hands and feet where the cuticle 
is thickest. 

Clinical Types. — In addition to the cases of moderate severity 
described above there are 

1. Mild Cases. — In these the onset is abrupt, but the temperature 
rises only to 102° or 103° F., and may reach normal within four or five 



SCARLET FEVEH 



349 



days. The rash may not involve the face and may be only faint and 
transient over the body. The throat symptoms are usually slight. 

Such cases may easily be overlooked, especially when they occur in 
adults. They are important not only because they may transmit the 
disease in its severer forms, but also because they may be followed by 
a serious nephritis or other complication. 

2. Severe Cases. — The period of incubation is short; the onset violent ; 
the rash appears early, is pronounced and widespread, and the fever is 
high and protracted (two to three weeks). Delirium alternates with 
periods of stupor ; the pulse grows steadily feebler and more rapid ; the 
throat symptoms are very severe. Complications are very common and 
the child is likely to die either of the severe toxemia or of the 
complications. 




Fig. C8 — A, desquamation of scarlet fever on neck and chest; B, desquamation of scarlet fever on back. 



3. The Malignant Form. — The onset is violent, usually with con- 
vulsions and persistent vomiting; the fever is extremely high (105°- 
108°), and the pulse very rapid and feeble. Delirium soon gives place 
to coma and the child dies within forty-eight hours, overwhelmed by 
the poison of the disease. The rash is faint, irregular or may be 
wanting altogether. Exceptionally the eruption is hemorrhagic and 
accompanied by bleeding from the mucous surfaces. IMalignant scarlet 
fever is fortunately rare and is seen only during severe epidemics. 

4. The Anqinose Form. — This name is given to those distressing 
cases in which the throat inflammation is extremely severe. There is 
from the outset rigidity and tenderness of the neck and jaws and pain 
and difficulty in swallowing. The pharynx, fauces, tonsils and uvula 
are intensely red and upon the third or fourth day show a membranous 
exudate which may extend into the posterior nares or larynx. There 
is an offensive, sanious discharge from the nose and mouth ; the cervical 



350 



THE INFECTIOUS DISEASES 



glands are greatly swollen, and there is often a diffuse cellulitis of the 
neck. Necrosis and sloughing of the tonsils or soft palate or cervical 
glands may occur. The constitutional disturbance is extreme and the 
cases are usually fatal. 

Surgical Scarlet Fe\^r. — ^Vhile it is undoubtedly true that puer- 
peral women and persons with fresh wounds are peculiarly susceptible 
to scarlet fever, it is also true that many of the fevers seen in these cases 
are not true scarlet fever, but septicemia with an erythematous rash. 

Relapses. — A recrudescence of the fever, eruption, angina and other 
symptoms is occasionally seen during convalescence. 

Complications and Sequelae. — These are numerous and \ery 
important. 

Nephritis. — A slight albuminuria is seen in most of the cases dur- 
ing the active stage and has little significance. True acute nephritis 
may occur at any time, but is usually seen during desquamation. It 
may occur as late as the sixth week. All grades of severity are met 
with. The mild cases recover promptly. In the severer forms many 
of the children die of uremia or else the acute symptoms subside and 
the disease persists as a chronic nephritis. 

Otitis Media. — Suppurative inflaromation of the middle ear, due 
to infection through the Eustachian tube, is a common and important 
•complication, since it may result in permanent deafness or in mastoiditis, 
thi'ombosis of the lateral sinus, meningitis or brain abscess. Its fre- 
quency bears a direct relation to the severity of the throat inflammation. 
It is often bilateral. 

Arthritis. — A sjTiovitis, serous or purulent, is occasionally seen. 
Usually it affects several large joints and closely simulates acute ar- 
ticular rheumatism. 

The Heart. — Simple acute endocarditis, pericarditis (serous or 
purulent) and acute myocarditis are occasional complications. The for- 
mer often results in permanent deformity of the valves. 

The Luxgs. — Bronchopneumonia is found in most of the fatal cases. 
Pleurisy with effusion and empyema are both not uncommon. 

Cellulitis of the neck is a grave complication, seen especially 
with the anginose form. The abscess usually begins in the cervical 
lymph-nodes. 

True diphtheria sometimes develops during convalescence. The 
membranous angina so frequently seen, however, is usually associated 
with the streptococcus pyogenes and is therefore not true diphtheria. 

Diagnosis. — Confusion is likely to occur only in atypical cases such 
as those of the malignant form, in which the rash is irregular or is 
lacking, and of the anginose form, which may readily be mistaken for 
diphtheria. The diagnosis is to be made quite as much by the abrupt 
onset, the vomiting, the rapid rise of temperature and the very early 
appearance of the rash as by the character of the rash itself. This may 
be simulated by a number of other rashes, especially by those of septi- 
cemia, urticaria, measles, rubella, acute exfoliative dermatitis and by 



PLATE II. 



A B 




The Pathognomonic Sign of Measles (Koplik's Spots). 

A. The discrete measles spots cii the buccal or labial mucous membranes, showing the isolated rose- 
red spot, with the minute bluish-white centre, on the normally colored mucous membrane. 

B. Shows the partially diffu.se eruption on the mucous membrane of the cheeks and lips; patches of 
pale pink interspersed among rose-red patches, the latter showing numerous pale bluish-white spots. 

C. The appearance of the buccal or labial mucous membrane when the measles spots coniplotciy 
coalesce and give a diffuse redness, with the myriads of bluish-white specks. The exanthema on the skin 
is at this time generally fully developed. 

D. Aphthous stomatitis apt to be mistaken for measles spots. Mucous membrane normal in line. 
Minute yellow points are surrounded by a red area. .Always discrete. — Med. News, June 3, 1899. 



SCARLET FEVER 



351 



those caused by certain drugs, such as quinine, sodium salicylate, bella- 
donna, potassium iodide and antipyrine. In all of these conditions 
there are lacking the characteristic onset and early symptoms of scarlet 
fever, and the universal distribution of the rash. 

Prognosis. — The average mortality is from 10 to 15 per* cent. It 
varies, however, in different epidemics between five and forty per cent. 
The disease is especially fatal in children under two years. Death may 
be caused by the intense systemic poisoning, by sepsis from the severe 
angina, by such complications as bronchopneumonia and severe otitis 
media or by post-scarlatinal nephritis. 

Prophylaxis. — The child should be immediately isolated and no one 
but the nurse and physician should enter the sick-room. Other chil- 
dren in the family should be at once sent away. The three chief sources 
of contagion are the patient, the nurse, and the room. The patient will 
usually have to be kept in his room for six weeks. If desquamation is 
not then complete, or if there still persist discharges from the nose, 
throat, ear or from abscesses, he must be isolated until these have ceased. 
The danger from desquamation can be diminished by keeping the skin 
anointed with earbolized vaseline or some bland ointment. Before he 
leaves the sick-room every part of the child's body should be thoroughly 
scrubbed with soap and water several times and sponged with a 1-5000 
solution of corrosive sublimate. The urine and feces are to be disin- 
fected as described under Typhoid Fever. Discharges from nose, ears, 
abscesses, etc., should be received into surgical gauze or absorbent cotton, 
which can be burned. Soiled linen is soaked for one hour at least in a 
1-20 solution of carbolic acid and afterward boiled for two hours in 
water. (See also Appendix, p. 583.) 

The nurse should be kept apart from the rest of the family as much 
as possible and should change her clothing and disinfect her hands and 
face upon leaving the sick-room. The physician should wear in the room 
a gown and head covering. 

Before the sick-room is occupied it should, if possible, be stripped 
of its carpet, hangings and upholstered furniture. After the patient 
has left the room it should receive most thorough disinfection. The 
walls if painted can be washed with bichloride solution, otherwise they 
are best cleaned by being rubbed down with moist bread, the frag- 
ments of Avhich can be burned. The floor and woodwork are scrubbed 
with a solution of bichloride of mercury 1-1000. If possible books and 
toys should be burned. Clothing, carpets, mattress, upholstered furni- 
ture are best disinfected in the steam disinfecting stations provided by 
most large cities. If this is not feasible, exposure to direct sunlight for 
a number of days is probably the most useful measure. The method so 
much in vogue of simply fumigating the room and all its contents with 
sulphur is of exceedingly doubtful value. Formaldehyde gas is more 
trustworthy, but to be effective must be used in larger quantities than 
most of the lamps now on sale will generate. 

Treatment. — This consists in careful nursing, the prevention of 



352 



THE INFECTIOUS DISEASES 



complications and the combating of individual symptoms. The child 
is at once put to bed and kept there until the temperature has been 
normal for a week. A fluid diet (chiefly milk) is maintained for the 
same period. The room must be well ventilated, but great care should 
be exercised to prevent the patient from taking cold. The child should 
be made to drink very freely of water throughout the whole of the 
disease. The danger of nephritis can be further diminished by the 
moderate use of saline laxatives and by keeping the skin active by means 
of warm baths. The urine should be examined frequently. 

The nose and throat are kept clean by free irrigation with some 
mild antiseptic or with normal salt solution. If the throat symptoms be 
severe, however, this is of little avail in preventing otitis. The burning 
and itching of the rash can be somewhat relieved by keeping the skin 
well protected by vaseline or boric acid ointment. 

Hyperpyrexia and the severe nervous symptoms are best treated by 
warm tub baths, which can be gradually cooled to 85° F. or less as indi- 
cated, or by packs. An ice-cap to the head is useful when the cerebral 
symptoms are marked. 

In severe cases when the heart weakness threatens life stimulants 
must be used freely. Of these alcohol, in the form of brandy or whiskey 
well diluted, is perhaps the best. It is usually well borne and can be 
given in relatively large amounts (as much as three ounces in twenty- 
four hours to a child of four years). Strychnine and digitalis are also 
valuable. The local treatment of the throat in the anginose form is 
that described under Diphtheria. 

If otitis media develop, the drum membrane must be watched closely 
and puncture resorted to if the accumulation of fluid be marked. 

Nephritis, if it appear, is to be treated as though it were a primary 
condition. (See p. 160.) 

Suppuration of the lymph-glands or the cellular tissue of the neck 
demands immediate incision. 

MEASLES 
(Morbilli. Rubeola) 

Definition. — Measles is an acute, highly contagious disease of child- 
hood which manifests itself by coryza, conjunctivitis, moderate fever 
and a diffuse rose-red maculopapular eruption. 

Etiology. — The disease is one of the most widespread and highly 
contagious known. It is transmitted usually by direct exposure; con- 
veyance by means of a third person or by fomites being much less com- 
mon than in scarlet fever. Susceptibility is almost universal in children, 
but the disease is rarely seen in infants of less than six months. It 
may occur in adults. Most of the epidemics occur during the colder 
months of the year. The contagious period extends from the beginning 
of the catarrhal symptoms to the end of desquamation, the contagious- 
ness being very pronounced even before the appearance of the eruption. 
Protection is not always secured by one attack. 



PLATE III. 

The Eruptions of Mkasles and Scarlet Fever. 




MEASLES 



353 



Morbid Anatomy. — The only lesions constantly present are those 
of the cutaneous eruption and the catarrhal inflammation of the nose, 
conjunctivae, larynx, trachea and large bronchi. Bronchopneumonia is 
regularly present in the fatal cases. 

Symptoms. — The incubation occupies quite regularly from ten to 
fourteen days. 

Invasion. — The onset is usually gradual, the symptoms being those 
of a severe cold; sneezing, catarrhal rhinitis, suffused and reddened 
eyes, hoarseness and hoarse cough. The temperature rises within two or 
three days to 103° or 104° F. and the child is fretful, listless and drowsy. 
Not infrequently the temperature, instead of rising steadily, will fall 
on the second or third day and rise again with the appearance of the 
rash. (See Fig. 69.) Occasionally the onset is more abrupt and violent, 
but a distinct chill is rare. The stage of invasion lasts from two to 
four days. 




Fig. 69. — Temperature curve of severe measles. The crosses mark the development of the eruption. 
One day of slight fever preceded the period charted. 



Eruption. — The rash appears on the third or fourtli day and shows 
first on the forehead, neck and behind the ears. In many cases on the 
day before the eruption small red spots with bluish- white centers may 
be seen scattered over the mucosa of the palate and cheeks (Koplik's 
spots) (see Plate II). The rash at first consists of a few small, macular 
spots of a deep rose-red color, which soon change to soft, velvety papules 
and become much more numerous, spreading slowly over the face, trunk, 
arms and legs in the order named and' occupying three or four days 
in the process. The papules arrange themselves in large groups which 
are apt to take a crescentic or rounded outline and many of which fuse 
into diffuse large blotches (see Plate III). By the time the rash appears 
on the legs it has begun to fade upon the face. Meanwhile the fever and 
all the catarrhal symptoms have persisted and there are intense itching 
and burning of the skin and often diarrhea. With the fading of the rash 
the temperature falls rapidly and the other symptoms gradually subside. 
23 



354 



THE INFECTIOUS DISEASES 



Desquamation begins soon after the rash has disappeared (usually 
on the eighth or ninth day) and lasts from five to ten days. It is always 
fine and bran-like (furfuraceous) in character. 

Not all the cases run the typical course described. There are mild 
CASES in which the fever is slight and the rash and the catarrhal symp- 
toms less intense : and severe cases in which the fever is high and 
protracted and which are usually complicated by bronchopneumonia. 
IMalignant cases, in which the child is overpowered by the intensity of 
the poison, are fortunately rare. There is also a severe form called 
"black measles" marked by a dark colored and hemorrhagic rash and 
often by bleeding from the mucous membranes. 

Complications and Sequelae. — The chief complications are broncho- 
pneumonia, pseudo-membranous laryngitis and phar^Tigitis, otitis media, 
pleurisy, enterocohtis, and ulcerative or gangrenous stomatitis. 
Nephritis is rare. Of the sequelae tuberculosis (general, pulmonary or 
glandular) is much the most important. Chronic conjunctivitis and 
chronic enlargement of the lymph-glands are not uncommon. 

Diagnosis. — The chief differential points in distinguishing measles 
from the other exanthemata are the gradual onset, the marked catarrhal 
sjTuptoms, the late appearance of the rash, its slow development and its 
large blotches with crescentic outlines. The Koplik spots upon the 
palate and buccal mucous membranes are also very suggestive. 

Prognosis. — Fatal cases are rarely seen in private practice among 
children over three years. Below this age the mortality is about ten 
per cent. In asylums and in tenements, however, the death rate is 
often much higher. Bronchopneumonia is the commonest cause of 
death. 

Treatment. — Prophtl^vxis. — Early isolation of the patient is most 
important. Children who have been exposed should be kept away from 
other children for sixteen days. The patient himself must be isolated 
for at least three weeks. The child should be kept in bed, and upon 
fluid diet, throughout the febrile period, and the room kept darkened 
and well ventilated. The ejes are to be kept clean by frequent bathing 
with a saturated solution of boric acid. The itching of the eruption 
may be lessened by the application of some bland ointment. During 
desquamation daily warm baths should be given. Troublesome cough 
may be relieved by ipecac and paregoric or by small doses of codeine 
(gr. 1/15-1/30). If the bronchitis be severe, counterirritation in the 
form of mustard pastes frequently applied to the chest is often of 
great value. The treatment of persistently high temperature, of severe 
nervous symptoms and of heart weakness is that described under Scarlet 
Fever. During convalescence great care is needed, not only to prevent 
the complications, but also to improve as rapidly as possible the child's 
physical condition, in the hope of thereby diminisliing the chance of 
bronchopneumonia and tuberculosis. Nutritious food, tonics, cod liver 
oil, etc., are needed and a change of climate is often desirable. 



DIPHTHERIA 



355 



RUBELLA 

(German Measles. Rbtheln) 

Definition. — Rubella is an acute contagious disorder characterized 
by a pronounced but variable rash, slight constitutional disturbance 
and the absence of complications. It was formerly much confused with 
measles and scarlet fever, from both of which, however, it is entirely 
distinct. 

The disease is only moderately contagious, occurs in epidemics and 
attacks adults as well as children. 

Symptoms. — The incubation period varies much, but is commonly 
from ten to fifteen days. 

In many cases no symptoms whatever are noticed before the rash 
appears. Usually, however, for a few hours before the eruption is seen, 
there are some headache, malaise, slight fever and perhaps a mild coryza. 
This stage of invasion is almost always less than two days. 

Eruption. — The rash often closely resembles that of measles; less 
frequently it is scarlatiniform. It appears first upon the face, spreads 
over the whole body within 24 hours, persists for two or three days and 
then fades rapidly. It is composed usually of minute pale red, slightly 
elevated spots, which, upon the face, may become confluent. Desquama- 
tion is very slight or altogether lacking. With the rash the temperature 
may reach 101° or 102° F. ; there is often a mild sore throat, some 
itching of the skin, and the posterior cervical lymph-glands are regu- 
larly swollen. Complications are almost unknown and the prognosis 
is uniformly good. 

Diagnosis. — It is frequently impossible, by the rash alone, to dis- 
tinguish German measles from true measles or from scarlatina. It 
differs from the former, however, in its very mild course, the absence of 
marked catarrhal symptoms, the early appearance of the rash, the 
absence of Koplik's spots, the swelling of the lymph-glands and the 
absence of complications; and from scarlet fever in its long incubation, 
its very mild onset and course, its mild throat sjonptoms, the glandular 
enlargement and its freedom from desquamation. 

No treatment but good nursing is required. It is necessary to insist 
upon isolation. 

DIPHTHERIA 

Definition. — An acute contagious disease caused by a specific micro- 
organism — the hacillus diphtheria^ and marked, usually, by a pseudo- 
membranous inflammation of the fauces, pharynx, nose or larynx and 
by constitutional symptoms due to the absorption of toxins. 

Careful bacteriological studies of diphtheria and its allied affections 
have demonstrated, first, that the bacillus di i)h I In rice does not always 
excite an inflammation with the production of a distinct false membrane, 
but may occasionally cause only a slight catarrhal process; and second, 
that such pseudo-membranous inflammations are sometimes caused by 



356 



THE INFECTIOUS DISEASES 



other bacteria than the diphtheria bacillus. The presence of this 
organism then, in any given case, is the only certain evidence that the 
disease is true diphtheria. 

For such pseudo-membranous inflammations as are caused by other 
bacteria Osier has suggested the term diphtheroid. 

Etiology. — Diphtheria has long been known as one of the common 
and important contagious diseases, and occurs endemically, epidemically 
and sporadically. It is endemic in most large cities, where from time 
to time also the cases multiply to such an extent as to constitute an 
epidemic. In the country it is seen chiefly in small epidemics. 

Predisposing Causes. — The disease is widely distributed throughout 
the world. It occurs at all seasons, but is most prevalent during the 
winter months. Children under ten years are much more liable to 
infection than are adults; the age of greatest susceptibility being from 
two to five years. Infants are rarely attacked. The disease is slightly 
conunoner in girls than in boys. Predisposition to the disease is greatly 
increased by such abnormal conditions in the throat as enlarged tonsils, 
adenoid growths or chronic naso-pharyngeal catarrh. The occasional 
association of true diphtheria with such diseases as scarlet fever and 
measles is probably to be explained in this way. 

The EXCITING cause is the 'bacillus diphtherice, known also from its 
discoverers (1883-1884) as the Klebs-Loffler bacillus. This is a non- 
motile, slender rod of medium length, straight or slightly bent and with 
rounded and often club-shaped ends. It stains peculiarly in that 
different parts of the organism often stain with different intensity and 
so give to it a somewhat beaded appearance. This tendency to varia- 
bility in shape and staining is a feature of much practical value for the 
identification of the organisms. The bacilli grow most readily upon a 
medium composed chiefly of blood serum and, at body temperature, the 
colonies become visible within 10 or 12 hours. The Klebs-Loffler bacillus 
is very tenacious of life and may live for many weeks or months even 
under unfavorable conditions. The organisms are always present in 
the throats of those ill of the disease and are especially numerous in the 
superficial layers of the false membrane. In the deeper parts of the 
mucous membrane and in the circulating blood they are but rarely 
found. 

Transmission. — Diphtheria is transmitted only by means of these 
bacilli and every case has its origin in some other. The manner of such 
communication is, however, often very obscure and difficult to trace. 
The bacilli are given off in the secretions and discharges of the mouth, 
throat and nose and especially in the fragments of false membrane. 
Such discharges reach the mouth and throat of other persons either 
directly, as in the act of coughing or kissing, or indirectly through the 
medium of toys, bedding, clothing, dishes, etc. The organism thrives in 
milk and certain epidemics have been traced to this source. Drinking 
water is believed never to carry the contagion. Physicians and nurses 
in attendance upon cases of diphtheria are frequently infected, and 



DIPHTHERIA 



357 



even when not ill, their throats have occasionally been found to contain 
diphtheria bacilli. In patients convalescent from the disease, the bacilli 
sometimes remain in the throat and retain their virulence for several 
weeks or even longer, and such persons probably play an important part 
in the dissemination of the disease. The same is true of those cases of 
diphtheria which develop little or no pseudo-membrane and which are 
therefore often mistaken for simple sore throat. Cats are subject to 
a similar pseudo-membranous affection and diphtheria may perhaps 
sometimes be conveyed in that way, although the identity of the two 
diseases has not yet been thoroughly established. Sewer gas and 
defective drainage are no longer regarded as important causative agents. 
Although second attacks are not common the disease does not confer 
the same degree of immunity as do most of the other contagious diseases. 

Toxin. — The diphtheria bacillus in its growth produces a chemical 
poison — a toxin — which is readily absorbed from the site of the local 
lesion and is carried throughout the body by the blood. Most of the 
constitutional symptoms and severe visceral lesions have been shown 
to be due to the action of this toxin. 

Other hacteria are frequently found associated in the throat with 
Klebs-Loffler bacillus. Of these the streptococcus pyogenes is the most 
important. To it are due certain secondary suppurative processes and 
septicemias. 

Morbid Anatomy. — The diphtheria bacilli,, in the vast majority 
of cases, find lodgment upon, and excite an inflammation of, the mucous 
membrane of the upper air passages. In rare instances, however, the 
false membrane may be seen in the stomach, middle ear, conjunctivae, 
vagina or upon open wounds. The membrane most frequently appears . 
upon one or both tonsils and from these often spreads over the soft 
palate and uvula, and back to the lateral and posterior walls of the 
pharynx. It frequently extends also into the naso-pharynx and from 
there into the posterior nares and nose. In other eases the extension is 
downward to the epiglottis, larynx, trachea and bronchi. Not infre- 
quently the process begins in the nose or in the larynx. 

The false membrane differs greatly in color, extent and consistence 
in different cases and at different stages of the same case. The color 
is usually a dirty gray or yellow, but may be greenish, brown or almost 
white. The membrane may be thick, dense and firmly adherent or loose, 
friable and shreddy. Occasionally the inflammation is marked by ex- 
tensive sloughing not only of the mucous membrane but of the deeper 
structure as well, so that even large blood-vessels may be eroded and the 
tissues of the neck become the seat of extensive and deep-seated suppura- 
tion. This grave condition is especially likely to occur when other 
bacteria, such as the streptococcus, are acting in conjunction with the 
diphtheria bacillus. 

Histologically the process is an acute exudative inflammation with 
necrosis of the epithelial cells of the superficial layers of the mucous 
membrane. The false membrane consists of a meshwork of fibrin 



358 



THE INFECTIOUS DISEASES 



enclosing leukocytes, red cells and masses of dead epithelial cells. These 
dead cells undergo a peculiar hyaline transformation (coagulation 
necrosis), and constitute an essential feature of the process. 

Other Lesions. — Post-mortem examination shows that the cell 
necrosis is by no means confined to the mucous membrane. It is pro- 
duced by the toxin rather than by the direct action of the bacilli, and 
is often found in the cervical lymph-nodes, in the parenchyma of the 
heart, kidneys and liver and in the peripheral nerves. In fatal laryn- 
geal cases the lungs always show areas of atelectasis and of broncho- 
pneumonia. 

Symptoms. — The clinical picture of diphtheria varies greatly, and 
depends not only upon the site and severity of the local process, but also 
upon the amount of toxin produced and absorbed. It is to the con- 
stitutional effects of this toxin that many of the gravest s^miptoms are 
due. 

The INCUBATION PERIOD is rarely longer than one week and usually 
lasts only from two to five days. 

Invasion. — This is apt to be mild and insidious rather than abrupt 
and violent, although exceptions to this rule are common. In very 
young children the onset is frequently abrupt, with a sudden rise of 
temperature, vomiting or convulsions. Usually, however, headache, 
malaise, loss of appetite, slight fever and slight sore throat mark the 
beginning of the disease. 

1. Pharyngeal Diphtheria. — Mild Type. — The membrane appears 
upon the tonsils and is often confined to them, being usually small in 
amount. It may, however, extend somewhat over the faucial pillars or 
the lateral pharyngeal wall. The onset is mild and the constitutional 
symptoms slight. The fever ranges between 100° and 302° F. The 
throat feels uncomfortable, there is some pain on swallowing, the lymph- 
glands below the angle of the jaw are tender and swollen. The child 
may not feel sick enough to be in bed. The throat looks somewhat red 
and swollen; the membrane at first ma}" be only a film or may be made 
up of several small white spots closely resembling those of simple fol- 
licular tonsillitis. When well developed it forms a gray or whitish 
patch firmly adherent to the mucosa. If forcibly detached it leaves a 
bleeding surface, which is promptly re-covered by false membrane. The 
membrane lasts from three days to a week or more. By the time of its 
disappearance the child is usually convalescent. Complications are 
infrequent. This type is frequent among older children and adults. 

Severe Type. — The symptoms at first are similar to those of the mild 
form, but the membrane shows a tendency to extend, and soon covers 
the fauces, uvula and pharyngeal wall. Often, too, it spreads to the 
posterior nares or to the larynx. The tonsils and uvula are much 
swollen and there is a free secretion of mucus. Although usually the 
temperature is not high (100°-103° F.), the constitutional symptoms 
soon become marked. The prostration is extreme; the pulse grows 
progressively weaker and more rapid (110-140) ; there is apathy, stupor 



DIPHTHERIA 



359 



or great restlessness; pallor is pronounced; there may be vomiting or 
diarrhea. The blood shows a rapidly progressive anemia and usually 
a well-marked leukocytosis ; the cervical lymph-glands are much swollen ; 
the urine is albuminous and often contains casts and blood cells. In rare 
instances the patient is fairly overwhelmed by the intensity of the 
poisons and dies within two or three days. Usually the toxemia is- most 
pronounced from the fifth to the tenth day. Death is common during 
this period and not infrequently comes suddenly and unexpectedly. It 
is usually attributed to heart failure from myocardial degeneration or 
from neuritis of the cardiac nerves. Recent studies have seemed to 
show, however, that this collapse is due primarily to paralysis of the 
vaso-motor control of the vessels rather than to derangement of the 
heart itself. If the patient survives, the membrane begins to loosen and 
come away during the second week, and convalescence, often slow and 
tedious, begins. 

A distressing and grave form of the disease is that known as septic 
diphtheria, in which the local symptoms are especially severe (being 
due to a mixed infection by the diphtheria bacillus and the streptococcus 
pyogenes), and in which evidences of septicemia or pyemia develop. 

Cases Without a Membrane. — A small but important class of cases 
are those which show only a catarrhal inflammation of the throat, with 
no membrane whatever, or with only a few white spots upon the ton- 
sils which cannot be distinguished from those of simple follicular ton- 
sillitis. And yet these are cases of true diphtheria, are liable to the 
usual complications of the disease and are capable of spreading 
contagion. 

2. Nasal Diphtheria. — The infection may be primary in the nose, 
but it usually occurs by extension from the naso-pharynx. The mem- 
brane may completely fill the nose and may be seen at the anterior nares. 
The local symptoms are those of obstruction of the nares, together with 
a nasal discharge which is usually profuse, thin, acrid and often blood 
tinged. The constitutional sjnuptoms are as a rule very severe and the 
glandular swelling marked. There may be an extension of the mem- 
brane through the Eustachian tube to the middle ear or through the 
lachrymal duct to the conjunctiva. 

3. Laryngeal Diphtheria. — (Memhraiwus croup). — It is fully 
established that membranous laryngitis, or croup, is in the vast majority 
of cases true diphtheria. The chief exceptions to this rule are those 
cases which develop in the course of such diseases as scarlet fever and 
measles and which are usually due to the streptococcus pyogenes. The 
membrane commonly reaches the larynx by extension from the pharynx. 
Less frequently the process begins in the larynx. It frequently extends 
downward along the trachea and may even invade the finer subdivisions 
of the bronchial tree. 

The laryngeal symptoms begin rather gradually with hoarseness or 
whispering voice, a harsh, "cr()ni)y" c(mgh and a modei'ate rise of 
temperature. The breathing gradually becomes more labored and within 



360 



THE INFECTIOUS DISEASES 



a day or two the symptoms of laryngeal stenosis are usually well marked. 
Each inspiration is accompanied by a stridulous sound, by dilatation of 
the nostrils and by a sinking in of the tissues of the neck and of the 
epigastrium. Expiration also is difficult and sometimes stridulous. The 
child struggles for breath, becomes pale and then cyanotic and finally, 
in many cases, dies of suffocation within two or three days. If the 
larynx alone is involved the toxemic symptoms are usually slight. In 
favorable cases the obstruction is not severe and after from two to five 
days the membrane loosens and is coughed up and the child goes on to 
recovery. 

Complications and Sequelae. — Bronchopneumonia is very com- 
mon, especially in cases with involvement of the larjTix and in septic 
diphtheria. Acute nephritis is also frequent. Toxic myocarditis is 
doubtless responsible for certain of the instances of heart failure. Sup- 
puration OF cervical glands may occur, especially in the type of septic 
diphtheria. Otitis media is occasionally met with, and such skin erup- 
tions as erythema and urticaria are not \ery uncommon. Other com- 
plications are rare. The chief sequel to diphtheria is paralysis. This 
is due to local or multiple neuritis caused by the diphtheria toxin, and 
is met with in from 10 to 15 per cent, of the cases. The paralysis usually 
shows itself during convalescence. It may appear as early as. the end 
of the first week or as late as the sixth week. 

The commonest form of paralysis is that of the soft palate. It is 
recognized by a nasal quality of the voice, by the regurgitation of fluids 
through the nose during the act of swallowing and by the immobility 
of the palate during phonation, etc. It is usually associated with anes- 
thesia of the parts and sometimes with paralysis of the muscles 
of the pharynx or larj^nx. There may be paralysis of the eye muscles, 
both intrinsic and extrinsic, with the resulting loss of accommodation, 
strabismus, ptosis, etc. Paralysis of the heart may be sudden or may 
develop somewhat gradually with the symptoms of weakness, sjmQope, 
pallor and a feeble and irregular pulse which is either abnormally slow 
or very rapid. It is frequently fatal. Disturbance of respiration is 
usually due to paralysis of the diaphragm. The breathing is labored 
and of the costal type and there may be distressing, even fatal parox- 
ysms of dyspnea and cyanosis. 

IMuLTiPLE NEURITIS is uot uucommou and shows itself by paralysis 
of the extremities, loss of tendon reflexes and disturbances of sensation. 
]\Iarked ataxia may be a feature even when the actual paralysis is slight. 
In general both local and multiple neuri tides are of short duration and 
recovery usually takes place within a few weeks or months. 

Diagnosis. — While in most cases a careful weighing of the clinical 
evidence alone will suffice to make a correct diagnosis, there are never- 
theless many doubtful and obscure cases which can only be cleared up 
by bacteriological examination. This is especially true of cases in 
which there is little or no membrane : of inflammations primary in the 
nose or lar,ynx, and of throat affections associated with scarlet fever 



DIPHTHERIA 



361 



and measles. The clinical diagnosis is based upon both, the consti- 
tutional symptoms and the local appearances. The constitutional symp- 
toms in diphtheria are apt to begin gradually, to be mild at first and 
to be most pronounced several days after the onset. In follicular ton- 
sillitis and in diphtheroid affections the onset is usually more abrupt 
and severe and the general symptoms of shorter duration. Of the local 
signs, those which point most strongly to diphtheria are the uniform, 
firm character of the membrane, its grayish color, the difficulty of 
detaching it, its tendency to extend beyond the limits of the tonsils and 
the small amount of redness and swelling of the surrounding mucous 
membrane. If there is also involvement of the nose or larynx the case 
is almost certainly diphtheria. Membranous inflammation in a child 
is much more likely to be diphtheria than in an adult. A bacteriolog- 
ical EXAMINATION should always be made when possible. For this pur- 
pose a sterile swab is first rubbed over the suspicious areas in the throat 
and then over the surface of a tube or plate of Loffler's blood-serum. 
This is then kept at 100° F. for 12 or 15 hours and smears from the 
visible colonies are made, stained in the usual way and examined 
microscopically. A diagnosis can sometimes be made from stained 
smears made directly from the throat, but the cultural method is much 
more certain and satisfactory. 

Prognosis. — The mortality ranges from 10 to 20 per cent. It varies 
enormously with the age of the patient, the character of the epidemic, 
the location of the membrane, etc. The disease is most fatal in young 
children; in laryngeal cases, in cases of septic diphtheria, and in those 
in which the toxic symptoms are pronounced. Every case of diph- 
theria is serious and the prognosis should always be guarded, since in 
even the mildest cases there exists the possibility of sudden heart fail- 
ure or other grave complications. Since the introduction of the anti- 
toxin treatment the mortality, in cases in which it has been used early, 
has been reduced to less than 5 per cent. 

Prophylaxis.— Since the infectious material is spread only through 
the discharges of the mouth and nose, the prevention of contagion is 
not difficult if only intelligent care is exercised. Every suspicious case 
should be isolated at once until the diagnosis is made certain. Since 
it is the mild and unrecognized cases that are responsible for much of 
the spread of the disease rigid isolation and disinfection should be car- 
ried out as described under Scarlet Fever. The bacilli often remain 
in the throat for some days, or even for several weeks, after the dis- 
appearance of the membrane, and during this time there is danger of 
conveying the disease. Throat cultures, when possible, should be made 
from time to time and the patient kept in quarantine as long as they 
show the bacilli to be present. If such bacteriological examinations are 
impossible quarantine should be maintained in mild cases for at least 
ten days, in severe cases for at least three weeks, after the disappearance 
of the membrane. The well children in the infected household must be 
kept from school and from mixing with other children. 



362 



THE INFECTIOUS DISEASES 



Treatment. — GeneRx\l Management. — All cases, even the mildest, 
^should be kept in bed until convalescence is well established. In the 
sick-room fresh air, free ventilation and an equable temperature are 
essential. The diet should be fluid — milk, broths, whey, etc. — and 
should be given at two-hour intervals. AVater should be freely given. 
Care must be taken that the child be not too frequently disturbed hy 
,the various therapeutic measures employed. 

Drugs. — It is doubtful if any drug known has any direct, favorable 
influence upon the course of the disease. The tincture of the chloride 
of iron and the preparations of mercury which formerly were much 
used have been largely given up. Stimulants are needed in most of 
the cases during the latter part of the disease and should be adminis- 
tered freely when the heart shows signs of weakness. Alcohol and 
strychnine are the drugs chiefly to be relied upon. In sudden heart 
failure strychnine subcutaneously is of great value. During convales- 




FiG. 70. — Method of wrapping a patient for nasal irrigation or intubation as practiced in the Willard 
Parker Hospital, New York City. (After Nicoll.) 



cence iron, cod liver oil, or other tonics are usually required, as the 
anemia is apt to be severe. 

Local Treatment. — Efforts to destroy the bacilli by strong anti- 
septic applications are ineffective and often do positive harm. Clean- 
liness, however, is greatly to be desired. To this end the nose and naso- 
pharynx are freely and frequently irrigated and the mouth and throat 
sprayed with some bland fluid or mild antiseptic such as normal salt 
solution, saturated boric acid solution, half strength Dobell's solution, 
hydrogen peroxide, etc. (See Figs. 70 and 71.) In older children a 
gargle of very weak (1-10,000) bichloride of mercury may be used. 
The pain and discomfort of the throat are often mitigated by the use of 
external applications of heat or cold. 

Serum Treatment. — By the brilliant investigations of von Behring, 
Roux and others a specific method of treatment has now been developed 
by which the mortality has been greatly reduced and the disease robbed 
of many of its terrors. This treatment is based upon the fact that by 
the injection into an animal of repeated and gradually increasing 



DIPHTHERIA 



363 



amounts of the diphtheria toxin there is developed in the blood of the 
animal a chemical body — an antitoxin — which will neutralize the effects 
of a definite amount of the toxin. In this way animals may be im- 
munized against enormous doses of the diphtheria poison. Moreover, 
the blood-serum of such immunized animals is. capable of neutralizing 
the effects of the diphtheria toxin in the human body, and also of con- 
ferring at least a temporary immunity against the disease to healthy 




'Fig. 71. — Method of nasal irrigation. The receptacle containing the irrigating solution should be 
sufficiently above the patient's head to give a gentle flow. (After Nicoll.) 

individuals. In practice the blood-serum of highly immunized horses 
is used after having been sterilized and tested as to its antitoxic strength. 
This strength is estimated in units, each unit representing 100 times 
the quantity of serum needed to neutralize the minimal fatal dose of 
diphtheria toxin for a guinea-pig weighing 250 grammes. 

Diphtheria antitoxin is used for two distinct purposes: first, as 
a CURATIVE MEASURE in thosc suffering from diphtheria, and second, 



364 



THE IXFECTIOUS DISEASES 



to FURNISH IMMUNITY to healthy persons exposed to infection. The 
curative dose varies from 1000 to 5000 units, according to the age 
of the patient and the severity of the symptoms. For children over two 
years of age 2000 or 5000 units is the usual amount. If no improve- 
ment is noticed within twelve hours this dose should be repeated. Rarely 
a third injection may be required. A large, carefully sterilized hyipo- 
dermic syringe is used and the serum is slowly injected into the sub- 
cutaneous tissue of the back, chest or buttock. It is desirable for various 
reasons to use the most concentrated serum obtainable. The beneficial 
effects of antitoxin are seen chiefly in cases in which it is used early 
in the disease, i.e., within the first 48 hours. In all severe cases, and 
even in mild cases in young children, it should be used at once and 
without waiting for the bacteriological diagnosis. The good effects are 
usually promptly seen in the lessening of the local redness and swelling, 
in the loosening of the membrane and in the improvement in pulse, tem- 
perature and the constitutional symptoms. This is true of the lar^Tigeal 
cases as well as of those of pharyngeal diphtheria. 

Serious symptoms, as a result of the use of antitoxin, are rare. Skin 
eruptions, such as erji:hema or urticaria, together with a rise of tem- 
perature and joint pains, occasionally develop from seven to ten days 
after the injection. They are unpleasant but never serious. Xo harm 
results from the use of antitoxin even if the disease proves not to be 
diphtheria. A few cases of sudden death following the administration 
of diphtheria antitoxin are on record. Some at least of these deaths have 
been due to the poisonous effect of the proteid contained in the horse 
serum (anaphylaxis). Danger from this source is lessened by the use 
of concentrated sera. Recent studies suggest strongly that asthma is 
a similar anaphylactic reaction and clinical experience has shown that 
diphtheria antitoxin is especially dangerous to asthmatics. Antitoxin 
should therefore not be given to asthmatic patients. Since a latent 
asthmatic tendency may well exist in a child without the knowledge of 
either parents or physician, it is advised in all cases to test the sus- 
ceptibility of the patient by tiie injection of a minute quantitj^ of the 
serum (0.5 c.c.) and to follow this by the full curative dose in ten or 
^ fifteen minutes if no reaction develops. Susceptible individuals react 

almost instantly to even the minute quantity named. 

Immunizing doses of from 300 to 500 units should be given at once 
to all children who have been exposed to infection. By such a dose 
practically complete immunity is secured for a period of at least sev- 
eral weeks. Nurses or other adults exposed to infection may be protected 
in like manner. 

Treatment of Laryngeal Cases. — Every case of primary mem- 
branous laryngitis should receive a prompt and liberal dose of antitoxin 
(5000 units or more), for in no type of diphtheria are the results more 
gratifying, and the dose repeated in 12 hours if necessary. The air that 
the child breathes should be warmed and moistened by the use of a steam 
croup kettle near the bed. Calomel fumigations are recommended. A 



DIPHTHERIA 



365 



tent is made over the child's crib and filled with the fumes of calomel 
and these are inhaled for 15 or 20 minutes at intervals of from one 
to three hours. Ten or fifteen grains of calomel are placed in a pan 
or on a metal sheet and heated hy an alcohol lamp placed beneath, great 
care being taken to avoid fire. In the intervals between the fumigations 
the tent should be removed and the room aired. If the stenosis is 
progressive and becomes serious, intubation or tracheotomy should be 
resorted to. Of late years the former has replaced tracheotomy and 
is now the measure usually employed. 

Intubation. — The indications for intubation are such a degree of 
dyspnea from laryngeal stenosis as to cause definite cyanosis with retrac- 




FiG. 72. — The O'Dwyer intubation set. 1. The introducer. 2. The extractor, the tip turned up 
instead of down. 3. The set of hard-rubber tubes, adapted to children from 1 to 12 years of age. 
4. The mouth-gag. 5. The scale to determine the age for which each tube is adapted. 

tion of the soft tissues in the episternal notch, the supraclavicular spaces, 
and the epigastrium. In some instances care is required to distinguish 
laryngeal stenosis from the cyanosis and dyspnea occasioned by broncho- 
pneumonia. 

The INSTRUMENTS and procedure are those devised by Joseph 
O'Dwyer (see Fig. 72). The child may be held in either of the two 
positions shown in Figs. 73 and 74. Care is especially necessary to have 
the head and neck in a straight line. The child being in the proper 
position, the tube indicated by its age and size is selected, a silk thread 
run through the ''eye" of the tube and the tube secured by its metal 
obturator on the handle of the introducer. Taking the introducer in 
the right hand and sitting or standing as indicated in the illustrations, 



366 THE INFECTIOUS DISEASES 

the operator introduces the left index finger till its tip rests upon the 
arytenoid cartilages and holds the epiglottis flat upon the base of the 
tongue. The tip of the tube is then passed along the anterior surface 
of the finger as a guide until it reaches the upper aperture of the 




Fig. 73. — Intubation in the sitting position. Note the manner of holding the patient, steadying the 
head and'controlHng the mouth-gag. (After Nicoll.) 



larynx. It is then thrust home, i.e., into the laiynx, by raising the right 
hand and pressing the introducer flat on the tongue, while at the same 
time the left index finger is slipped onto the head of the tube, and presses 
it firmly into the larjmx, while the introducer and the obturator of the 
tube are withdrawn, leaving the tube in the larynx. 



DIPHTHERIA 



367 



The tube is often coughed out in the course of a day or two and not 
required again. If stenosis returns the tube must be replaced. In a few 
cases repeated introductions must be made. 

If the tube remains in the larynx extraction is practiced after two 
or three days. 

In this procedure the positions of patient and operator are the same 
as in the introduction of the tube. The left index finger is passed down 
upon the arytenoid cartilages and the high rear edge of the tube. The 
tip of the extractor is then made to follow the finger into the lumen 
of the tube. When the tip engages in the lumen the pressure of the 




Fig. 74. — Intubation in the supine position. Note again the manner of steadying the head and con- 
trolhng the mouth-gag. (After Nicoll.) 



thumb upon the lever of the extractor opens the blades of the bill of the 
instrument and clutches the tube, which is then withdrawn by revers- 
ing the movement of intubation. 

In infants without molar teeth both these procedures may be prac- 
ticed without a mouth-gag, but in other children the gag is necessary. 
In infants after the introduction of the tube the thread running through 
the eye may be carried into the angle of the mouth secured on the 
cheek by a bit of adhesive plaster, and later used to extract the tube. 

Older children are likely to pull out the tube by the thread and 
it must therefore be cut and Avithdrawn after the introduction, the 



368 



THE INFECTIOUS DISEASES 



primary purpose of it being to serve for withdrawal of tlie tube in 
case of unsuccessful attempts to place the tube in the larynx. O'Dwyer 
always insisted upon the necessity of previous training on the cadaver 
before attempting intubation in the living and few indeed can succeed 
without such training. 

The early use of antitoxin has almost done away with the need of 
either intubation or tracheotomy, so that intubation is in this country 
now a rare procedure and tracheotomy for the stenosis of diphtheria 
is almost unheard of. 

Feeding Intubated Patients. — The tube interferes with the closure 
of the larjnix by the epiglottis and liquids often enter the larynx and 
give rise to severe coughing. To avoid this semi-solid foods should be 
used rather than liquids, and if the difficulty is pronounced, the Cassel- 
bury position should be tried. In this the child is laid upon the back 
upon the nurse's lap, the head being allowed to fall over one side, and 
the child is fed in this position either from a spoon or through a tube. 

DIPHTHEROID INFLAMMATIONS 
(Pseudo-Diphtheria) 

Definition. — The term diphtheroid is applied to those pseudo-mem- 
branous inflammations of the throat and upper air passages which are 
excited by bacteria other than the Klebs-Loffler bacillus. The strepto- 
coccus pyogenes is the germ usually dominant. It is often associated 
with the staphylococcus aureus or alhus. Such inflammations are by no 
means uncommon, and occur in both a primary and a secondary form. 

The PRIMARY cases begin usually as a tonsillitis. A false membrane 
soon appears, however, which may be indistinguishable from that of 
true diphtheria. Often it is of a yellowish color and more friable and 
less firmly adherent than that of diphtheria. It shows also much less 
tendency to extend beyond the limits of the tonsils. The redness and 
swelling of the throat, however, are usually more pronounced than in 
true diphtheria. Clinically the cases show a more abrupt onset, a 
higher temperature and a shorter course than diphtheria. These primary 
cases are rarely fatal — the mortality being not more than two or three per 
cent. 

The SECONDARY TYPE is sccu as a complication of such diseases as 
scarlet fever, measles, typhoid, etc. True diphtheria itself may be 
associated with such diseases, but this happens only infrequently and 
then usually during convalescence rather than in the active stage of 
the primary disease. While some of the cases of the secondary type may 
be mild the form is as a rule severe. The membrane is often extensive, 
may involve the nose or i ^nx and is often associated with sloughing 
and deep suppuration, ' is well illustrated in the anginose type of 
scarlet fever. In many eases a condition of general septicemia or 
pyemia develops. This secondary type differs greatly in its prognosis 



WHOOPING-COUGH 



369 



from the primary one. Most cases are very severe and prolonged and 
as many as one-third or one-half of them prove fatal. 

Diphtheroid inflammations seem to be slightly, if at all, contagious 
and so do not require the rigid and long isolation necessary in diphtheria. 
Nevertheless, such cases should be kept apart from other children and 
the discharges from the throat and nose disinfected. 

Local treatment should be along the lines suggested for diphtheria. 
The use of antistreptococcus serum has hitherto not been satisfactory. 

WHOOPING-COUGH 
(Pertussis) 

Definition. — Whooping-cough is a contagious disease of epidemic 
character occurring in childhood, whose chief feature consists in se- 
vere paroxysms of coughing which terminate in a shrill inspiratory 
^' whoop " and are often followed by vomiting. 

Etiology. — The disease is one of the common affections of child- 
hood and is distributed widely over the globe. Although met with spo- 
radically, it occurs chiefly in epidemics which are commonest in the 
winter and spring and are frequently associated with epidemics of 
measles. Most of the cases are found in children under ten years of age. 
Young infants are often attacked, as are sometimes also adults. It is 
commoner in girls than in boys. The disease is highly contagious 
throughout its whole course. It is contracted usually through close con- 
tact, but may be conveyed by fomites or even by means of a third per- 
son. The exciting cause is still unknown. Several micro-organisms 
have been found in the sputum, but none has yet been proven to be the 
real cause of the disease. Second attacks are not common. 

Morbid Anatomy. — No characteristic lesions are found after death. 
There is probably always a catarrhal inflammation of the larynx, trachea 
and larger bronchi, which, however, does not explain the peculiar parox- 
ysmal character of the symptoms. The tracheal and bronchial lymph- 
glands are often found enlarged and the fatal cases show such com- 
plications as bronchopneumonia, vesicular or interstitial emphysema, and 
meningeal congestion and hemorrhage. Miliary tuberculosis is also a 
frequent finding in fatal cases. 

Symptoms. — The period op incubation is commonly of about ten 
days' duration. Only rarely is it less than seven or more than fourteen. 

The symptoms are conveniently divided into three stages: the catar- 
rhal, the paroxysmal, and the stage of decline. 

Catarrhal Stage. — The onset is gradual and insidious with the 
symptoms of a mild bronchitis or ''cold." T je are slight fever, irrita- 
bility, coryza, and a dry cough which is not p??^oxysma.l. Examination 
of the chest shows nothing more than an occasional bronchial or moist 
rale. 

PAROXYSMATi Stage. — In the course of a week or ten days the cough 
24 



870 



THE INFECTIOUS DISEASES 



becomes more spasmodic and the characteristic whoop appears. The 
paroxysms consist of a series (ten to twenty) of short, hard coughs com- 
ing in rapid succession and ending in a long, deep inspiration which has 
a crowing or whooping sound. These coughs and whoops raay be re- 
peated several times and the paroxysm ends by the child raising a plug 
of tenacious mucus from the larynx or trachea and often by vomiting as 
w^elL During the coughing there are great congestion of the head and 
neck, enlargement of the veins, suffusion of the eyes and often marked 
cyanosis, all of which are relieved after the crowing inspiration. Such 
paroxysms vary in number from five or six to forty or fifty in the twenty- 
four hours. These attacks may be excited by eating, drinking, crying, 
etc., but are often spontaneous and are usually especially frequent dur- 
ing the night. The constant vomiting seriously interferes with nutri- 
tion and the child grows thin, pale and listless. The temperature, as a 
rule, remains normal and the chest presents no characteristic physical 
signs. The blood regularly shows a marked leukocytosis with an increase 
in the proportion of lymphocytes. This stage usually lasts from two to 
four weeks, but in severe cases may be much longer. Occasionally the 
paroxysms are indistinct and slight and the whoop may be lacking alto- 
gether. 

Stage of Decline. — The spasms of coughing grow less frequent and 
severe and finally cease, although some cough persists for weeks. This 
stage usually lasts from three to four weeks and the whole period of 
the disease is commonly from eight to twelve weeks, but may be much 
longer. 

Complications. — Bronchopneumonia is the most common and seri- 
ous complication, especially in young children. It may be tuberculous. 
Vesicular emphysema is frequent. Rupture of air vesicles may result 
in extensive infiltration of the tissue with air. Hemorrhages, from the 
violent coughing efforts, are common in the nose and conjunctiva and 
may occur in the bronchi, ears, meninges, etc. Convulsions are met with 
in young children and may be fatal. Hemiplegia, aphasia, disturbances 
of sight, etc., occur rarely. The persistent vomiting? may result in 
great anemia and emaciation. Diarrhea is not uncommon. 

Diagnosis. — This rests upon the history of exposure, the severe 
spells of coughing, the peculiar whoops, the long-continued cough with- 
out fever or physical signs in the lungs. In mild and doubful cases a 
leukocytosis with a marked lymphocytosis would point strongly toward 
pertussis. In a child an acute bronchitis which fails to improve under 
rational treatment should always be regarded with suspicion. 

Prognosis. — The disease is very fatal in infants, chiefly from bron- 
chopneumonia or convulsions. In older children among the better 
classes, the mortality is slight, but the patients are often long in recover- 
ing from the exhausting effects of the disease. Tuberculosis is not infre- 
quently a sequel. 

Treatment. — Patients should be carefully kept away from other 
children and from school throughout the disease, but should not be con- 



MTOIPS 



371 



fined to a room. Fresh air is of the greatest importance and they should 
be kept out of doors as much as possible. The feeding demands much 
attention, because of the great tendency to vomiting, and everything 
should be done to maintain the general health. Plain, nutritious food 
should be given in small quantities, and at short intervals. 

Xo method of treatment is known by which the disease can be cut 
short. All that can be hoped for from drugs is to diminish the fre- 
quency and severity of the paroxysms. No one drug seems to act 
best in all cases. The following list includes some of the more important 
drugs with the average daily amount needed for a child of two years: 
Quinine gr. vi, antipyrine gr. viii, tincture of belladonna m. xv, sodium 
bromide gr. xx, chloral gr. x, bromoform m. v. 

Inhalation of creosote, carbolic acid, formaldehyde, cresolin, etc., is 
sometimes useful, and a change of air is often of benefit. 

MUMPS 
(Epidemic Parotitis) 

Definition. — A specific contagious disease characterized by inflamma- 
tion of the parotid glands and a tendency to metastatic inflammation of 
the sexual organs. 

Etiology. — Mumps is a disease chiefly of older children, but is occa- 
sionally seen in infancy and in adult life. It appears usually in epi- 
demic form and during the winter months. Contagion occurs, as a 
rule, only after close contact. Transmission through a third person 
or by fomites is rare. The nature of the contagium is unknown. Boys 
seem rather more susceptible than girls. 

Morbid Anatomy. — The lesion is an acute exudative inflammation 
of the parotid gland and its surrounding connective tissue, which ter- 
minates regularly in resolution. Suppuration is rare and accidental. 
Occasionally the other salivary glands may be involved. 

Symptoms. — The incubation period is quite regularly from two to 
three weeks. In mild cases pain is often the first symptom. In the 
severer form the local symptoms are usually preceded by a day or 
two of malaise, joint pains, headache and fever. 

The fever in such cases may reach 103° or 104° F., and lasts for 
several days. In mild cases it is very slight. The local symptoms begin 
as a rule with pain in the parotid region, followed promptly by swell- 
ing of the gland, which in two or three days reaches its height. The 
swelling is located chiefly below and in front of the ear and when 
marked, as it often is, displaces the lobe of the ear and gives to the face a 
singular and ludicrous expression (see Fig. 75). The swelling is boggy 
and tender, but not red. Both glands are commonly affected; the signs 
in the second one appearing usually a day or two after those of the 
first. The pain is felt in the glands, in the throat, and often in the 
ears, and is made worse by swallowing and by the presence of tart 



372 



THE INFECTIOUS DISEASES 



substances in the mouth. Often the jaws cannot be widely opened. The 
saliva is frequently much diminished. The swelling subsides in from 
five to ten days, while the constitutional symptoms are usually of much 
shorter duration. 

Complications. — In males beyond the time of puberty orchitis is a 
common complication. It may affect one or both testicles. It appears 
late in the disease, lasts four or five days and ends in resolution. It 
may be followed by atrophy of the testicle. In girls inflammation of 
the vulva, the breasts and the ovaries sometimes occurs. Rarely cerebral 
symptoms such as delirium and convulsions appear. IMeningitis, deaf- 
ness, nephritis, multiple neuritis and endocarditis are possible compli- 
cations. 




Fig. 75. — Mumps: Note how the swelUng extends upward in front of the lobe of the ear. 

Diagnosis. — The disease is usually easily recognized. It is to be 
distinguished from the secondary form of parotitis, which is usually 
suppurative. Occasionally it may be confused with swelling of the 
cervical lymph-nodes. 

Prognosis. — Mumps regularly terminates favorably and usually runs 
a mild and short course. Rarely death may occur from some compli- 
cation. 

Treatment. — Patients should be kept away from other children and 
from school for at least a week after the swelling has entirely subsided. 
Rest in bed is needed during the febrile stage. If there be much pain 
moist heat applied to the gland is usually comforting. Fluid diet or soft 
foods should be used when there is much pain and difficulty in swal- 
lowing. 



MUMPS 



373 



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374 



THE INFECTIOUS DISEASES 



SEPTICEMIA AND PYEMIA 
(Blood Poisoning) 

Definition. — Septic diseases are those caused by the invasion of the 
blood and tissues generally, by pyogenic bacteria or their toxic products. 
Chief among these pus-forming agents are the streptococcus pyogenes and 
staphylococcus pyogenics aureus. 

Three types of septic disease are recognized: (1) Septic Intoxication 
(Sapremia) ; in which the bacteria are confined to the local lesion and 
in which the general symptoms are caused altogether by the absorption 
and dissemination of the bacterial toxins. 

(2) Septicemia {Bacteremia) ; in which the bacteria themselves 
gain entrance to and multiply in the blood and. tissues. The term 
septicemia is also sometimes used to include septic intoxication. 

(3) Pyemia or Septico-pyemia; in which in addition to a septi- 
cemia there is the development of metastatic abscesses. 

SEPTIC INTOXICATION 

The constitutional disturbance in every form of local purulent intiam- 
mation, in which the causative bacteria are not disseminated through- 
out the hody, is an instance of septic intoxication. Empyema, puru- 
lent otitis media, appendicitis, erysipelas and certain forms of puerperal 
infection are familiar examples. The severity of the symptoms depends 
upon the nature of the toxin, the amount produced and especially upon 
the rate of absorption. The symptoms are chiefly fever, headache, ,thirst, 
anorexia, prostration, rapid pulse and, usually, leukocytosis. Practically 
it is often very difficult to distinguish between the severer forms of 
septic intoxication and a true septicemia or bacteremia. In the 
former case the symptoms should subside promptly upon the subsidence 
or removal of the local inflammatory process. When, however, the bac- 
teria have entered the general circulation no such close relation is seen 
between the constitutional symptoms and the state of the local infection. 

SEPTICEMIA 

Etiology. — Any local infection, however small and apparently insig- 
nificant, may be the starting point of a septicemia. Among the more 
important of such causes are puerperal infection of the uterus, acute 
osteomyelitis, acute otitis media with its complications of mastoid inflam- 
mation and septic thrombosis of the lateral sinus, post-mortem and other 
infected wounds, suppurative appendicitis, gonorrhea, liver abscess, 
etc. A very important class of septicemias is that in which during life 
(and even sometimes after death) the point of entrance of the bacteria 
cannot be determined — idiopathic or cryptogenetic sept ice ))iia. Such 
cases are by no means rare and come under the eye of the physician 
rather than the surgeon. They are prone to develop in those whose 
vital forces and powers of resistance are weakened by prolonged ill- 



SEPTICEMIA AND PYEMIA 



375 



ness, and are frequently seen in the last days of many chronic diseases 
and cachexias. 

Bacteria. — Of the exciting causes of septicemia the streptococcus 
pyogenes and the staphylococcus aureus and albus are much the most 
common. Other organisms less frequently met with are the pneumococ- 
cus, gonococcus, bacillus coli communis, bacillus pyocyaneus, bacillus 
aerogenes capsulatus, etc. The bacteria may gain entrance to the circu- 
lation by way of the lymphatics or by direct infection of the small 
veins in the vicinity of the primary focus either with or without an 
accompanying septic thrombosis. 

Morbid Anatomy. — The lesions found at autopsy are not peculiar to 
the disease. The blood is fluid and very dark, the viscera are con- 
gested and show parenchymatous degeneration, the spleen is swollen 
and soft, and hemorrhages into the serous membranes are common. 

Symptoms. — These appear usually within a very few days after those 




POUE 



I I ' ' ' ' ' I ' t ' I ' I ' I ' 1 M t I I I I I I I 
Fig. 76. — Temperature curve of septico-pyemia. 

of the local infection. The symptoms are often ushered in by a severe 
rigor and sweat, which may be repeated at irregular intervals through- 
out the illness. The fever is high and very irregular, often rising to 
105° or 106° F., and dropping suddenly to normal or below. (See Fig. 
76.) There are marked and increasing prostration, a very rapid, small, 
soft pulse and a dry tongue. The mind may remain clear, but if the 
symptoms last for many days a typhoid state " usually develops with 
muttering delirium or dulness and apathy. A severe diarrhea is 
common. The skin assumes a peculiar yellowish pallor or there may 
be distinct jaundice. Hemorrhages are frequently seen in the skin 
and mucous membranes. The blood shows a rapidly progressive anemia 
and, in almost all cases, a marked polymorphonuclear leukocytosis. By 
proper methods the bacteria can usually be demonstrated in the cir- 
culating blood. 

The course varies much. The severest cases are fatal within two or 
three days. Most of the cases last from five to ten days and not a few 



376 



THE INFECTIOUS DISEASES 



of these are fatal. In those cases which recover convalescence is apt 
to be slow and tedious. IMost of the very acute and severe forms of 
septicemia are caused by the streptococcus. Malignant endocarditis 
is a not very uncommon complication. 

Diagnosis. — If a cause for the general infection can be found, such 
as a septic uterus or a post-mortem wound, the diagnosis offers no diffi- 
culty. In the cryptogenetic cases the symptoms of chief diagnostic 
importance are the irregular temperature, the chills and sweats, the 
rapid prostration, the purpuric spots, the high leukocytosis and the 
presence of pyogenic bacteria in the blood. The conditions most likely 
to be confused with septicemia are malarial fever, the intermittent 
hepatic fever caused by impaction of a gall-stone in the common duct, 
malignant endocarditis, typhoid fever and certain types of pulmonary 
tuberculosis. 

Treatment. — The local infection should receive prompt and radical 
surgical treatment. The patient's strength should be maintained as 
well as possible by nutritious and easily digested food and by stimu- 
lants. The bacterial toxins should be diluted and their rapid elimination 
encouraged by high rectal irrigations or subcutaneous or intravenous 
infusions of normal salt solution, and by the free drinking of water. If 
the infectious agent is known to be the streptococcus pyogenes, anti- 
streptococcic serum may be tried. Or if the causative bacteria can be 
found in the blood, vaccines made after Wright's method may be em- 
ployed. 

PYEMIA 

A certain proportion of the cases of bacterial invasion of the blood 
and tissues (septicemia) is associated with the formation of multiple 
abscesses in the viscera and other structures. To these cases the name 
pyemia or septicopyemia is given. 

The ETIOLOGY of pyemia does not differ from that of septicemia in 
general. The sources of infection and the varieties of bacteria are the 
same. Metastatic abscesses are especially apt to develop, however, when 
the local infection sets up a septic thrombo-phlebitis in the neighbor- 
ing small veins. Fragments of the friable thrombus, containing the 
bacteria, are readily detached and may be carried by the blood stream 
to distant parts of the body and there excite local suppuration. Usually 
the septic emboli are carried first to the lungs, and these organs are 
therefore a favorable site for the secondary abscesses ; but often minute 
particles pass through the lung capillaries, enter the arterial system and 
may there produce septic infarcts and abscesses in the spleen, kidneys, 
brain, joints, muscles, subcutaneous tissue, etc. Septic infections of the 
endocardium may occur and from this malignant endocarditis other 
septic emboli may result. When the primary local infection is in the 
region drained by the portal vein {e.g., in the appendix) the emboli lodge 
chiefly in the liver and there set up multiple abscesses. The symptoms 
of pyemia are those of septicemia plus those of the metastatic abscesses. 



ERYSIPELAS 



377 



Chills and sweats are even more common than in septicemia alone and 
often show a striking periodicity, so that they may resemble closely those 
of intermittent malarial fever. The course of the disease is usually not 
so rapid as that of the most virulent type of septicemia and most of 
the cases last from one to three weeks. In some of the milder forms the 
course is still more chronic and the conditions may persist for several 
months. The prognosis in most cases is bad, although many of the 
chronic cases (usually staphylococcic infections) eventually recover. 

The DIAGNOSIS is made by the recognition of a septicemia and the 
appearance of metastatic abscesses. 

The TREATMENT of pyemia does not differ from that of septicemia, 
except that the abscesses, when they appear, demand surgical treatment. 

ERYSIPELAS 

Definition. — Erysipelas is an acute contagious inflammation of the 
skin caused by the streptococcus erysipelatis, an organism not distin- 
guishable from the streptococcus pyogenes. 

Etiology. — The disease is wide-spread and occurs endemically, spor- 
adically, and occasionally in small epidemics. It is commonest during the 
spring months and is seen at all ages and in both sexes. Chronic alco- 
holism, debilitating chronic diseases, unhygienic surroundings and un- 
cleanly habits are predisposing causes. Liability to the disease is much 
increased by the presence of open wounds and by the puerperal state. 
Under modern aseptic methods erysipelas has now become rare in the 
surgical wards where once it was a scourge. The streptococcus ery- 
sipelatis seems to be very closely related to, if not identical with, the 
streptococcus pyogenes. The cocci are found in great numbers in the 
lymphatics of the inflamed skin especially at and just beyond the spread- 
ing margin. Infection occurs probably always by inoculation of a 
wound or an abraded skin or mucous surface, although frequently the 
point of infection cannot be discovered. The germs may be carried by 
the hands of physicians and nurses, by instruments, dressings, fomites 
and, apparently, also by the air. Often it is impossible to trace the 
origin of the disease. 

Morbid Anatomy. — The process is a severe acute inflammation of 
the entire thickness of the skin, and often of the subcutaneous areolar 
tissue, with intense hyperemia and marked infiltration of the tissues 
with serum, leukocytes and fibrin. In severe cases cutaneous abscesses 
may develop. 

Symptoms. — The incubation period lasts from three to seven days. 
The ONSET is abrupt and sometimes violent. An initial chill is common ; 
there is frequently vomiting and the temperature rises rapidly to 103°- 
105° F. This is associated with headache, fever, pains and a rapid, 
bounding pulse. 

Local Symptoms.— In traumatic erysipelas the inflammation shows 
itself usually in the vicinity of the infected wound. In the idiopathic 



378 



THE INFECTIOUS DISEASES 



form the process, in most cases, appears upon the head or face, although 
it may begin at any part of the body. Within a few hours of the onset, 
in a typical case, a small area of skin on the cheek or over the bridge 
of the nose becomes red and swollen and this spot rapidly increases in 
size so that within twenty-four hours a considerable area of the face 
is involved. The affected skin is bright red, swollen, hot, shining and 
indurated. The advancing edge of the inflammation is sharply defined 
from the normal skin and is distinctly elevated. The process spreads 
rapidly to the forehead, ears, lips and often to the hairy scalp. The 
face is enormously swollen, the eyes are closed by subcutaneous edema, 
and the features are often quite unrecognizable. The process sometimes 
extends to the mucous membrane of the nose, mouth or throat. Fre- 
quently serum collects beneath the epidermis in small blisters or larger 
blebs and in severe cases there may be small cutaneous abscesses. In 
most cases of facial erysipelas the inflammation stops at the neck. A 




Fig. 77. — Temperature curve of erysipelas of moderate severity. 

migratory type is sometimes seen, however, in which it slowly extends 
from place to place until the greater part of the body has been covered. 
The inflammation lasts usually from five to ten days. During this time 
the fever persists, but falls rapidly to normal as the local process sub- 
sides. (See Fig. 77.) Albuminuria is common and there may be a 
troublesome diarrhea. In severe or protracted cases delirium or the 
so-called typhoid state " may develop. 

Complications. — A number of severe complications, such as pneu- 
monia, nephritis, edema of the glottis, malignant endocarditis, septicemia, 
pyemia and meningitis, are possible^ but fortnnately none of them is 
common. 

Diagnosis. — The marked constitutional disturbance and the char- 
acteristic local appearances (the bright red, swollen and indurated skin 
with its sharp, elevated margin) are the features of special diagnostic 
importance. 



ACUTE RHEUMATIC FEVER 



379 



Prognosis. — The disease is rarely fatal except in those suffering from 
severe surgical affections or in debilitated or alcoholic subjects. A form 
of the disease occurring in new-born infants from infection at the umbili- 
cus is very fatal. 

Treatment. — Isolation and disinfection are required as in the case 
of other contagious diseases. 

The constitutional symptoms are to be treated symptomatically. The 
patient's strength should be maintained by nutritious and easily digest- 
ible food and when necessary by stimulants such as alcohol or strychnine. 
Tr. ferri chloridi (m. xx-xl t.i.d.) has been much used, but its efficacy 
is doubtful. 

Local Treatment. — Ichthyol, in the form of 10 to 30 per cent, oint- 
ment, is perhaps the most satisfactory. Compresses soaked with satu- 
rated boric acid solution or a weak carbolic sohition (1-50) or with lead 
and opium wash often give much relief. Injections of carbolic solution 
(1-50) into the skin just beyond the inflamed margin have sometimes 
succeeded in limiting the inflammation. In many cases, however, the 
disease runs its self-limited course apparently uninfluenced by any 
method of treatment. In some cases repeated injections of antistrepto- 
coccic serum appear to have been beneficial and in a few instances have 
seemingly stopped the progress of the disease. 

ACUTE RHEUMATIC FEVER 
(Acute Articular Rheumatism) 

Definition. — An acute febrile disease, probably of infectious nature, 
characterized by multiple arthritis and a tendency to inflammation of 
the heart and of various fibrous tissues. 

Etiology. — Predisposing Causes. — Acute rheumatism prevails chiefly 
in temperate and moist climates. In this country most cases are seen 
during the late winter and spring months. In England, however, it is 
most frequent in the autumn. It occurs for the most part endemically, 
but occasionally appears in small epidemics. 

Age. — The disease is seen chiefly in adolescence and young adult life ; 
the great majority of cases occurring between the ages of fifteen and 
forty years. It is by no means infrequent in children between five and 
fifteen years, but is rare in infancy and in old age. 

Sex. — In children rheumatism is commoner in girls than in boys, but 
in adult life males are the more frequently attacked. 

Heredity plays a less important role than is popularly supposed, 
although a certain predisposition seems occasionally to be transmitted. 
The continued exposure to cold and damp, and to sudden changes of 
temperature, distinctly predisposes to the disease and it is frequently 
met with among coachmen, truckmen, bakers, laborers, etc. One attack 
does not provide immunity, but rather increases the liability to the 
disease. 

Bacteriology. — Various micro-organisms, in particular a micrococcus 



380 



THE IXFECTIOrS DISEASES 



resembling in many ways the streptococcus pyogenes, have been sug- 
gested as the cause of the disease, but for all of these satisfactory proofs 
are still lacking. Po^Titon and Paine have especially studied the prob- 
lem and have isolated from the local lesions an organism which they 
have called streptococcus rheumaticus and regard as the specific agent. 
The belief that rheumatism is an infectious disease is. however, almost 
universal. It has many points of similarity with septicemia and is looked 
upon by some as a modified form of that disease. The tonsils are now 
regarded as the probable portals of entry for the infectious agent. By 
some it is held that the symptoms are not caused by a single specific 
germ but may be produced, under certain conditions, by all the common 
pyogenic organisms. The older views that the disease was due to the 
accumulation in the tissues of lactic or uric acids (chemical theory), 
or to a primary disturbance of the nerr^e-centers controlling the nutri- 
tion of the joints (nervous theory), have been almost wholly abandoned. 

Morbid Anatomy. — The lesion of the joints is an acute exudative 
inflammation affecting both the s^Tiovial membrane and the peri-articular 
structures, the exudate consisting of serum and some fibrin. Only very 
rarely is the exudate purulent. From its character the inflammation is 
capable of, and usually undergoes, complete resolution, and permanent 
damage to the joints is very unusual. The most frequent lesion in the 
heart is an acute, simple endocarditis, leading usually to sclerosis and 
deformity of the valves. Acute pleurisy or -pericarditis (flbrinous or 
serous) and acute myocarditis are much less connnon. 

Symptoms. — In many cases there are for a day or two slight 
PRODROMATA sucli as malaisc, sore throat and vague joint pains. Often, 
however, the onset is abrupt, with pain and swelling of one or two 
joints and a rapid rise of temperature. A distinct chill is uncommon. 
Within 24 or 36 hours the disease is fully developed. The affected 
JOINTS are extremely painful, especially upon the slightest movement, 
and are swollen, somewhat reddened and exquisitely tender. There is 
usually only a moderate quantity of fluid in the joint cavity, much of 
the swelling being due to the inflammatory edema of the peri-articular 
tissues. The knees, ankles, elbows, wrists and shoulders are the joints 
chiefly affected. Less frequently the phalangeal joints are inflamed, as 
are rarely also the vertebral, sterno-clavicular and temporomaxillary 
articulations. 

The inflammation regularly attacks several joints-, and it is a very 
characteristic feature of the disease that these are involved somewhat 
in succession, the swelling and pain suddenly leaving one joint and 
appearing in another. 

The fever is usually only moderately high (102°-103° F.) . is irregular 
and is commonly associated with profuse sweating; the sweat being acid 
in reaction and having a sour, pungent odor. Sweat vesicles (sudamina) 
frequently appear over the skin of the trunk. The pulse is moderately 
quickened, the tongue moist and heavily coated, the bowels constipated 
and the urine scanty, high-colored, and very acid. The blood shows a 



ACUTE RHEUMATIC FEVER 



381 



very rapidly progressive secondary anemia and usually a distinct leu- 
kocytosis. The symptoms commonly last from ten days to two weeks, but 
recrudescences and relapses are very common and it is not rare to 
have the course, even when uncomplicated, protracted to five or six 
weeks. To some of these cases with a mild but very protracted course 
the term subacute rheumatism may properly be applied. 

Symptoms in Children. — The joint symptoms are usually much less 
conspicuous than in adults and may appear only in the form of ' ' growing 
pains " ; or they may pass altogether unnoticed. On the other hand, the 
cardiac manifestations are frequent and serious. They may appear 
before the joint symptoms or they may be the only evidences of the 
disease. The secondary anem.ia is often severe. 

Complications. — The Heart. — Acute endocarditis is the commonest 
heart complication. It occurs in from one-fourth to one-half of the 
cases. It is especially frequent in children and in those who have had 
several attacks of rheumatism. It is regularly of the simple type — 
ulcerative endocarditis being exceedingly rare. The mitral cusps are 
much more frequently attacked than are the aortic. The condition may 
manifest itself by some increase in the temperature and pulse rate and 
by some precordial discomfort, but very often it gives no symptoms by 
which it can be recognized. The physical signs also may be very mis- 
leading. A systolic murmur over the apex or base of the heart is by 
no means proof that an endocarditis exists, since the apical murmur may 
be caused by a temporary leakage of the mitral valve, due to muscular 
relaxation, and a murmur over the pulmonic area is often caused by the 
severe anemia. Often the nature of the murmur can be determined 
by observing its persistence or disappearance after recovery from the 
rheumatic attack. Acute endocarditis is in itself usually not a serious 
matter. Its importance lies in the fact that it is so frequently the 
starting point of a chronic sclerosing process which results in serious 
deformity of the valve. 

Pericarditis is much less common than endocarditis. The exudate 
may be either fibrinous or serous. It may terminate in recovery or death 
or may result in obliteration of the pericardial sac and in fibrous thick- 
ening. 

Acute MYOCARDITIS is occasionally met with. There is granular and 
fatty degeneration of the heart muscle, together with more or less exuda- 
tion of serum and leukocytes into the interstices. It frequently results 
in dilatation and in serious weakening 'of the heart action. 

Hyperpyrexia. — This is a grave but fortunately very rare compli- 
cation. It is apt to develop in the latter part of the attack and without 
apparent cause. The temperature may rise rapidly to 106° or 108° F., is 
usually associated with delirium and cardiac weakness and often ter- 
minates in coma and death. Delirium occasionally occurs without hyper- 
pyrexia. It may then result from the rheumatic poison itself or may 
be due to a complicating pericarditis or to the toxic effects of the salicy- 
lates. 



382 



THE INFECTIOUS DISEASES 



Skin Affections. — The frequency of siidamina has been mentioned. 
Erythema nodosum and erythema multiforme, urticaria and pur- 
pura are all occasionally met with. 

Rheumatic Nodules. — In children, and especially in those who have 
had several rheumatic attacks, there frequently develop subcutaneous 
fibrous nodules, varying in size from a small shot to a bean. They are 
usually seen over the extensor surface of the elbows, forearms and wrists, 
over the patella and shins and along the vertebral spines. As a rule they 
represent a severe type of rheumatic infection. They are much more 
common in England than in this country. 

Chorea. — Chorea is sometimes, though by no means always, a rheu- 
matic manifestation. It may appear before, with or after the joint 
symptoms. 

Lobar pneumonia and pleurisy^ are occasional complications. Acute 
tonsillitis and pharyngitis are very frequently present at the onset, 
and may occur at any time during the attack. 

Diagnosis. — The involvement of several large joints, the transient 
and migratory character of the inflammation, the fever and the sour 
sweat are the most characteristic features in adults. The history of 
earlier attacks or the presence of vahoilar disease or of subcutaneous 
nodules will lend support to the diagnosis. It is important to remem- 
ber that in children the joint manifestations are often inconspicuous and 
slight. A monarticular arthritis is almost never rheumatic. 

Gonorrheal arthritis; the acute manifestation of arthritis deformans 
and gout ; scarlatinal ' ' rheumatism ' ' and other forms of septic or pyemic 
arthritis, and acute osteomyelitis are the affections most likely to be 
confused wdth rheumatism. 

Prognosis. — Rheumatic fever is serious chiefly because of the fre- 
quency of the heart complications. The liability to these is much greater 
in children than in adults and is much increased by each fresh attack 
of rheumatism. Large and numerous rheumatic nodules are usually 
of bad omen. Death from hyperpyrexia is rare. 

Treatment. — The patient should be put to bed at once and should 
remain there until convalescence is thoroughly established. Because 
of the tendency to free sweating it is well to have him wear a 
flannel night-gown, and lie between blankets rather than sheets. 
Fluid diet, chiefly of milk, is needed during the febrile stage. Later 
the diet should be made liberal, foods of all kinds being allowed. Water, 
lemonade, etc., should be given freely. The inflamed joints should be 
painted with oil of wintergreen, methyl salicylate or equal parts of 
guaiacol and glycerine, and enveloped in a thick roll of non-absorbent 
cotton. Immobilization during the acute stage may help to relieve pain. 

Drugs. — Two modes of treatment are in vogue : that with the salicyl 
compounds and that with alkalies. The salicylates have the power of 
relieving the pain and lessening the temperature without apparently 
shortening the course of the disease or diminishing the danger of heart 
complications. This last the alkalies are believed to do, although they 



GONORRHEAL INFECTION 



383 



are much less efficient in relieving pain. The best results are obtained 
by combining: the two methods. Sodium salicylate is the preparation 
most in use. It should be given in full doses (gr. xv-xxx every three 
hours) until the pain is relieved or until deafness or ringing in the 
ears appears, when the doses should be reduced in amount and in fre- 
quency. The salicylate is best given by combining with it twice as much 
bicarbonate of soda. Each dose should be well diluted in plain or car- 
bonated water. If sodium salicylate is not well borne by the stomach 
salicin (gr. xx-xxx), oil of winter green (m. xv-xx) or aspirin (gr. 
xv-xx) are efficient substitutes. 

In the alkaline treatment potassium bicarbonate (gr. xxx) or citrate 
(gr. XX ) is administered every three or four hours until the urine 
becomes alkaline and is then given in amounts only sufficient to keep 
the urine neutral or slightly alkaline. 

If signs of cardiac mischief appear an ice bag, mustard pastes or 
blisters may be applied to the precordium and the patient must be 
confined to bed for a much longer period than usual, indeed until all 
signs of cardiac disturbance (except the murmurs) have disappeared. 

After the fever has subsided, iron, arsenic and the bitter tonics are 
useful. In the late stages counter-irritation, douching and massage to 
the joints may aid in hastening convalescence. Hyperpyrexia demands 
prompt and energetic treatment by cold baths. 

GONORRHEAL INFECTION 

The gonococcus is capable of exciting a number of disorders other 
than the common inflammation of the urethra. Some of these, such as 
epididymitis, prostatic abscess and cystitis in the male, and vaginitis, 
endometritis, salpingitis and peritonitis in the female, result from 
direct extension of the process from the urethra. In other instances, 
however, a general infection results from the absorption of the bacteria 
and their toxins from the point of primary infection and this may show 
itself as a virulent septicemia or it may excite local inflammations in 
various places remote from the primary focus; especially in the joints^ 
tendon sheaths, bursae, endocardium or pericardium. In every such 
instance it is probable that the gonococci themselves invade the blood 
stream, since they have repeatedly been demonstrated in the blood, m 
fluid from the infiamed joints and in the vegetations upon the heart 
valves; but it is possible that some of the milder disorders may be 
caused by the toxins alone. 

GONORRHEAL ARTHRITIS 

Inflammation of the joints complicates about ten per cent, of the 
cases of local gonorrheal infection. It is met with in both sexes, though 
far commoner in males, and has been known to result from gonorrheal 
ophthalmia in the new-born, and from gonorrheal vulvo-vaginitis in chil- 
dren. The condition manifests itself usually in the third or fourth week 



384 



THE INFECTIOUS DISEASES 



of the urethritis, but is sometimes seen much earlier or may deA^elop 
in the course of a chronic gleet. 

Morbid Anatomy. — The inflammation involves both the synovial 
membrane and the peri-articular structures (ligaments, tendon sheaths, 
fascia, bursas, etc.). The joint is filled with a serous, sero-fibrinous or 
sero-purulent exudate and the peri-articular tissues are swollen and 
edematous. Later there may be considerable formation of new con- 
nective tissue and subsequent fibrous thickening of the tissues about the 
joints. 

Symptoms. — Distribution. — Any joint may be attacked, but the 
knees, ankles and wrists are the ones commonly affected. Occasionally 
the smaller joints (phalangeal, temporomaxillary, sterno-clavicular, in- 
tervertebral, etc. ) are involved. In nearly half of the cases the inflamma- 
tion is confined to a single joint (monarticular form), and in many 
other instances to two joints. The polyarticular form is comparatively 
infrequent. 

The symptoms begin with pain, swelling and tenderness in the af- 
fected joint. The fever is usually not high (100°-102° F.), nor are the 
other constitutional symptoms marked. The joint is moderately swollen, 
and often only slightly reddened, but the edematous swelling extends for 
some distance above and below the joint and gives to the whole a fusi- 
form outline. The pain varies greatly in different cases, but it is usually 
very severe on motion or pressure. The active symptoms run a subacute 
course and last from two to six weeks, while the stiffness and disability 
often persist much longer. The tendency of the inflammation to move 
about from joint to joint, so characteristic of acute rheumatism, is 
usually quite lacking in this disease. In the polyarticular form the local 
inflammation is less severe and stiffness and pain on motion may be 
the chief symptoms. Sometimes the inflammation attacks chiefly the 
burs£e, tendon sheaths, fasciae or muscles^ with little or no involvement 
of the joints proper. 

Prognosis. — Most cases recover completely, although convalescence is 
frequently very prolonged and tedious. Occasionally the fibrous anky- 
losis may be complete and permanent. -Death may occur from an asso- 
ciated septicemia or endocarditis. 

Diagnosis. — This is not difficult except where no evidence of gonor- 
rhea can be obtained. In such cases a positive diagnosis can be made 
only by the finding of gonococci in the joint fluid. The subacute course, the 
involvement of a single joint, the absence of a shifting character to the 
inflammation, the degree of peri-articular involvement and the ineffective- 
ness of the salicylates are the chief distinguishing features from acute 
rheumatism. The condition may be confused with the acute manifesta- 
tion of arthritis deformans, and with gout, septic or tuberculous arthritis, 
osteomyelitis, etc. 

Treatment. — The salicylates and alkalies seem to have no effect what- 
ever. Tonics and reconstructives, such as iron, arsenic and cod liver 
oil, are, however, of distinct value. Both antigonococcus serum and 



TUMORS AND CYSTS OF THE BRAIN 



545 



Morbid Anatomy. — Many varieties of brain tumor are kno^vn — 
the common ones are tubercle, sarcoma, glioma, gumma and carcinoma. 
Tubercle occurs in the form of large, isolated and usually single tumors 
made up of masses of miliary tubercles or a single large tubercle as 
much as an inch or an inch and a half in diameter. Tubercle in the 
form of tumor is common in childhood, rare in later life. Gumma, on 
the other hand, never results from inherited syphilis, and is therefore 
very rare in childhood, but common in adult life. Sarcoma or car- 
cinoma may follow a primary growth elsewhere, but is usually primary 
in the brain. Glioma is a growth of neuroglia, and therefore peculiar 
to the nervous system. Cystic tumors of the brain may arise from 
parasitic infections, such as echinococcus or cysticercus. They are very 
uncommon in this country. Fibroma, angioma, myxoma, osteoma and 
other rare forms are known. 

In brain tumor the intracranial pressure is always increased, and 
if the skull is opened during life the dura bulges and its pulsation is 
diminished. The cerebral convolutions are regularly flattened. The 
ventricles often contain excess of fluid omng to obstruction of the venae 
Galeni by pressure. 

Symptoms. — These are both general and focal. 

General. — These are produced by the steadily increasing intra- 
cranial pressure. (1) Severe and persistent headache. (2) Mental 
disturbance. The disposition may change notably, and the patient be- 
come irritable, careless or indifferent. Memory is impaired and atten- 
tion fails. The patient may become dirty and untidy in his habits. 
(3) Vertigo and vomiting. Dizziness is common in any cerebral tumor, 
but is pronounced if the cerebellum is involved. Vomiting is frequent, 
and is usually projectile in type. (4) Slow pulse. The rate is slow, 
50 to 60, the pulse full and of high tension. (5) Convulsions. These 
may be general or of the Jacksonian t>pe. (6) Choked disk is present 
in 80 to 90% of brain tumors, and constitutes one of the most important 
signs of brain tumor. Amblyopia, defective vision or blindness may 
accompany the choked disk. The field of vision may be contracted with 
inversion of the color-fields, so that the field for blue may interlace with 
or lie within that for red. 

Focal Symptoms. — These depend upon the location. 

Frontal Region.- — Changes in temperament and mental activity are 
notable. Memory is impaired, ability to concentrate thought or to learn 
diminishes, and the patient becomes stupid and irritable, or uncon- 
trollable. 

'i'umors of the third left frontal convolution in right-handed per- 
sons cause motor aphasia with agraphia. In left-handed persons the 
tumor must be in the right hemisphere. 

Motor Area. — Tonic or clonic spasms of the muscles of some por- 
tion of the body are caused by tumors of the motor cortex. The 
spasms so caused occur at intervals and may terminate in general con- 
vulsions. The spasms always begin in those muscles whose centers of 
35 



546 



DISEASES OF THE BRAIN AND MENINGES 



representation are most affected by the tumor. Therefore, observation 
of these spasms as to their location at the beginning and the mode of 
spreading helps greatly in locating a tumor. Either extremity or the 
face may be affected. Paralysis or paresis may follow either in arm, 
leg or face, but cortical tumors rarely produce hemiplegia. Tumors 
involving the internal capsule or the motor tract beyond it may cause 
hemiplegia. 

Parietal Region. — Disturbances are not constant, but in many cases 
impairment of sensation or muscular sense follows. Word-blindness 
has been found to be due to lesion of the inferior parietal lobule (left) . 

Occipital Region. — Hemianopsia (bilateral homonymous) results 
from lesion of the occipital lobe. It may be unknown to the patient 
and must be tested for. 

Island of Reil. — Tumors of this area produce paraphasia — that is, 
disturbance of speech in which one word is regularly substituted for 
another. They may produce pressure upon the neighboring face cen- 
ters or even upon the internal capsule. 

Crus. — Tumor involving the cms should produce paralysis of the 
third nerve of the same side and the extremities of the opposite side of 
the body. The fourth nerve may also be involved. 

Pons. — Tumors in the upper part involve the third and fifth, in the 
lower part, the fifth, sixth, seventh and eighth. In this situation par- 
alysis of one or more of these nerves with loss of power on the opposite 
side of the body, so-called alternating hemiplegia, may result. 

Medulla. — The ninth, tenth, eleventh and twelfth nerves suffer Avith 
resulting difficulties in swallowing, in respiration, irregularity of the 
pulse, and paralysis of the tongue. Polyuria or glycosuria may also result. 

Cerebellum. — Because of the small space in which the cerebellum 
lies enclosed by the tentorium cerebelli, small tumors produce severe 
results. By compressing the fourth ventricle, tumors in this region 
cause distention of the ventricles above, and hence sjrtnptoms appear 
early. Staggering gait, vertigo and cerebellar ataxia, an incoordination 
which entirely disappears when the patient lies down, are marked. 
Nystagmus is frequently present. Knee-jerks are exaggerated. 

Diagnosis. — The s^nnptoms of steadily increasing intracranial 
pressure with the presence of choked disk are characteristic. Abscess 
of the brain must be excluded by the absence of any cause for suppura- 
tion, absence of any constant leukocytosis, or fever, or other con- 
stitutional symptoms of suppuration and the presence of optic neuritis. 
Brain abscess rarely gives rise to definite focal symptoms and then only 
late in the disease. 

Tubercular meningitis causes a more rapid development of sjTiiptoms. 
with hyperesthesia to light or sound, possibly tubercles in the chorioid. 
and without optic neuritis. Tubercle bacilli should be found in the 
spinal fluid. Chronic hydrocephalus in children is excluded by the size 
and shape of the head, the symmetiy of the rigidity or loss of power, 
absence of choked disk, and the comparative comfort of the patients. 



APHASIA 



547 



The Wassermann reaction is a valuable aid in the diagnosis of 
gumma. 

Course and Prognosis. — Gradual but steady increase in symptoms 
over one or two years is the usual history. Death at the end of two 
or three years results in nearly all cases. Gummata may be relieved, 
possibly cured by specific treatment. A few tumors have been success- 
fully removed b}'^ surgery, but only ten per cent, are operable, and of 
those operated upon but few survive. 

Treatment. — Active antisyphilitic treatment should be tried. The 
iodide of potassium is given in increasing doses up to 60 grains thrice 
daily. Inunctions of mercurial ointment or injections of mercury may 
be combined with the iodide. Careful study should be made in the 
effort to locate the tumor and operation undertaken, if it is accessible. 

APHASIA 

Definition. — Literally the word means loss of the power of speech, 
but in medicine includes all the disturbances of the use of language, 
either written or spoken, not dependent on intellectual failure or par- 
alysis of the vocal organs. Aphasia is a symptom of various cerebral 
lesions, not a disease in itself. The exact determination of the defect in 
speech is of material aid in the location of cerebral lesions, especially 
brain tumors. The subject is, therefore, of sufficient importance to be 
dealt with separately. 

To understand the different types of aphasia one must go back to 
the mental processes underlying the use of words in speaking or writ- 
ing. Every word has four points of relation or centers in the cerebral 
cortex. It can be heard or seen, it may be spoken or written. Thus, 
the auditory center lies in the temporal lobe, the visual center in the 
angular gyrus, the motor speech center in the third left frontal con- 
volution, and the center for writing in close relation to it in the centers, 
for arm and hand. Each of these actions depends upon the integrity 
of a definite area of the cortex, and also the normal use of words in 
speaking and writing depends not only upon integrity of these centers, 
but on their free communication with one another through the associa- 
tion fibers of the brain. 

The chief types of aphasia are described thus: 

1. Sensory Aphasia. — 1. Word-Deafness. — This condition is best 
illustrated by the common experience of forgetting names. Every one 
has at some time seen an acquaintance whom he sees, recognizes, per- 
haps knows all about, and yet cannot name. The memory picture of 
his name cannot be recalled and hence cannot be expressed. But if 
now the acquaintance says my name is John King, the recollection may 
still fail, if the defect is complete, but usually the sound of the 
name at once recalls its word picture and one recognizes its propriety 
and utters it. The condition here described is, of course, a matter of 
momentary forgetfulness, but in true word-deafness the condition 
persists. The patient is therefore unable to name familiar objects when 



548 



DISEASES OF THE BRAIN AND MENINGES 



brought to mind in any manner. In this condition there must be a 
cortical lesion involving the sound memory centers in the temporo- 
sphenoidal lobe. If the defect is but partial, the name of a thing can- 
not be recalled of one's self, but is recognized at once when heard. 
This auditory amnesia, as it is sometimes called, implies the integrity 
of the word-centers, but a defect, sub-cortical, in the fibers connecting 
them with other centers. This distinction between cortical and sub- 
cortical lesions is of importance mainly with reference to the possibil- 
ity of operating upon cerebral lesions such as tumors. 

2. Word-Blindness. — If this condition is complete word pictures are 
entirely lost. The thing seen is not recognized, and hence cannot be 
named. If the defect is partial only, the missing word picture, not 
reached by one route, the eye for example, can at once be recalled if 
the approach is made through another channel such as the ear. Thus 
a patient with complete word-blindness cannot recognize and name a 
bell, for example, when seen, but if it is rung in his ear he recognizes 
it at once and on request draws it in outline. He has the concept of a 
bell with its form, but it cannot be reached through the visual route. 

With relation to language complete word-blindness is shown by in- 
ability to read or write. The patient cannot read because he cannot 
recognize the characters before him. He cannot write because he cannot 
recall the shapes of the necessary letters. If the defect be onh^ partial, 
he can write at dictation or copy, although not understanding w^hat is 
written. 

Complete word-blindness indicates a cortical lesion in the region 
of the inferior parietal convolutions and angular gyrus. A partial 
word-blindness is produced by a sub-cortical lesion involving the fibers 
of association. 

3. Inter cortical Sensory Aphasia. — The fibers of association be- 
tween the auditory and visual word centers may be interrupted, pro- 
ducing a condition in which an object seen cannot be named, or if named 
cannot be recalled to mind, although recognized in both instances. This 
condition is produced by lesions of the association fibers connecting the 
temporal and occipital lobes. 

2. Motor Aphasia. — 1. Aphemia, or what is commonly called sim- 
ply aphasia, a condition in which although words or things are recog- 
nized by eye and ear, the patient cannot name them or speak because 
of inability to recall the muscular movement necessary. This happens, 
of course, independent of paralysis of the muscles of speech. 2. 
Agraphia, the condition in which one can name objects and speak as 
usual, but cannot write, because the memory of the movements neces- 
sary is lost. 3. Intercortical motor aphasia or paraphas'o. In this 
condition an interruption or interference with the association fibers 
connecting the motor and other word-memory centers results in a dis- 
turbance characterized by the use of the wrong word in speech or 
writing. The patient speaks or writes jargon. Paraphasia is particu- 
larly associated with lesions of the island of Reil. 



AMAUROTIC FAMILY IDIOCY 



549 



AMAUROTIC FAMILY IDIOCY 

Definition. — A rare affection of Hebrew children, characterized by 
mental impairment during the period of infancy, blindness and loss of 
power over much of the body. 

Etiology. — The causation is unknown. The disease occurs only 
among the Hebrews, and often affects more than one child in a family. 
It is not syphilitic. 

Morbid Anatomy. — A degenerative process is found affecting all 
the nerve-cells of the brain and cord. The degeneration affects particu- 
larly the body of the cell and the dendrites, not the axis cylinder. The 
changes in the cell may be slight or so complete that the cell is disin- 
tegrated. Sachs thinks the disease due to congenital deficiency of the 
nervous system, such that after three or four months of normal life, 
the cells yield to the ordinary demands of life and disintegrate. 

Symptoms. — These are briefly summed up by Sachs as: (1) Mental 
impairment during the first few months of life leading to complete 
idiocy. (2) Paresis or paralysis, either flaccid or spastic, of the greater 
part of the body. (3) The reflexes may be deficient, normal or in- 
creased. (4) A diminution of vision terminating in absolute blind- 
ness. (5) Marasmus and death before the age of two years. 

Various other symptoms, such as increased sensibility to touch or 
sound, nystagmus, strabismus, or convulsions, have been noted in some 
cases. 

Diagnosis. — This rests upon the mental impairment, the blindness 
and the ophthalmoscopic examination, which shows, in the region of the 
macula lutea, a bright cherry-red spot, an absolutely pathognomonic 
sign. (See Plate VII.) Treatment is of no avail. 

FUNCTIONAL NERVOUS DISEASES 

ACUTE DELIRIUM 
(Typhomania. Brain Fever. Bell's Mania) 

Definition. — An acute delirium or mania accompanied by fever, 
regularly fatal, without adequate organic lesions. 

Etiology. — Emotional excitement, injury, toxemia and infection are 
given as causes. In most instances no satisfactory explanation is to 
be had. 

Morbid Anatomy. — The meninges are congested, but the brain 
appears normal. Microscopically Osier found some exudation of leu- 
kocytes about the vessels and in the lymph-spaces. 

Symptoms. — The onset may be preceded by several days of restless- 
ness, irritability and insomnia. The onset is usually marked by fever, 
102° to 104° F., with some increase in the pulse and prostration. Wild 
delirium or an active mania develops easily. Hallucinations are vi\id, 
the patient talks or sings incessantly, and keeps in constant motion. 



550 



FUNCTIONAL NERVOUS DISEASES 



Such acts as salaaming may be repeated endlessly. The patient may 
straggle with his attendants, but rarely injures anyone but himself. 

A typhoid-like condition is developed with fever, a dry-brown 
tongue, rapid pulse, marked prostration, and rapid emaciation. At the 
end of a week or ten days the patient dies in collapse. 

Diagnosis. — Typhoid fever must be excluded by absence of the 
characteristic roseola and the enlargement of the spleen, and by the study 
of the leukocyte count, the Widal reaction, and blood cultures. Pneu- 
monia can be excluded only by the absence of the usual symptoms and 
repeated careful physical examinations. Delirium tremens presents a 
distinct etiology, characteristic hallucinations, and the active tremor of 
tongue and hands. 

Acute meningitis may be excluded by the absence of rigidity of the 
neck and Kernig's sign, and by the results of lumbar puncture. It is 
evident that, the diagnosis of acute delirium can hardly be safely ven- 
tured before the autopsy reveals the absence of lesions sufficient to 
account for the disease. 

Treatment. — Blood-letting has been recommended in the early 
stages. The general treatment must be that of typhoid fever. The 
bromides gr. xxx t. i. d. may be given for excitement or hyoscin in doses 
of 1/100 gr. Dram doses of the fluid extract of ergot every two hours 
are recommended. 

PARALYSIS AGITANS 

Definition. — A chronic nervous affection marked by muscular weak- 
ness, tremors and rigidity. 

Etiology. — Two-thirds of the patients are men. The disease rarely 
begins before forty. Exposure, privation and nervous strain appear 
to favor its development. Numbers of cases were observed during the 
siege of Paris and the war of the rebellion. 

Morbid Anatomy. — No distinctive lesions have been found. Brawny 
patches in the skin have suggested myxedema, and the theory that 
lesions of the parathyroids were related to the disease has been ad- 
vanced. 

Symptoms. — The onset is either sudden or gradual. Usually the 
weakness, stiffness and tremor appear in one hand or arm, then the 
other. All four extremities and even the head may be affected. When 
fully developed the clinical picture includes: 

1. The tremor, the most striking symptom. It is a rapid tremor, 
four to eight oscillations per second, usually most marked in the hand. 
The movement of the fingers suggests pill-rolling. Flexion and exten- 
sion of the wrist or slight rotation may be combined with the finger 
movements. It may show clearly in the hand-writing. It usually is 
present at rest, and disappears on effort, but in some cases accom- 
panies voluntary action — i.e., is inieniional. In the foot the tremor 
causes rapid flexion and extension at the ankle, and the toe taps the 
floor as in clonus. 



ACUTE CHOREA 



551 



2. Rigidity of the muscles is the most pronounced feature of the 
disease. Rigidity precedes or accompanies the tremor. Passive motion 
may be impeded, but the reflexes are not increased and ankle clonus 
is not found. The facies becomes mask-like. The eyes are held 
open and fixed in one position, the whole head being revolved in- 
stead of moving the eyes from side to side. The patient rarely 
winks. The neck muscles are rigid as in torticollis, but both sides 
are involved, and the face is not turned to either side. The body 
is bent forward at the hips and the spine is bowed forward. In 
the hands similarly the fingers and wrists are usually flexed. Speech 
and gait are often characteristic. In speaking the patient hesi- 
tates a moment, then hurries the words out and stops abruptly. In 
like manner the patient, rising from a chair, halts a moment, then with 
the body bent forward advances with short, hurried steps, as though 
the feet were trying to overtake the body. In rare cases the patient 
actually falls forward. 

3. The mental state is marked by inertia. The patients are dull, 
sluggish, talk little and are indifferent. Dementia is often sug- 
gested, but when roused the patients show complete possession of their 
faculties. 

4. Sensory disturbances. The patients complain of sensations of 
heat or cold, but respond normally to tests. Vasomotor changes may 
be indicated by flushing of the skin, increased sweating or salivation. 

5. Muscular atrophy is not marked and no electrical changes are 
present. 

Course. — The disease is chronic and incurable, lasting many years. 
Periods of improvement may occur. 

Diagnosis. — In a typical case the diagnosis can be made on sight. 
The attitude of the body, the gait, the mask-like face, and muscular 
rigidity as well as the tremor are characteristic. Disseminated sclerosis 
is marked by earlier onset, scanning speech, and nystagmus. The 
tremor is regularly intentional. Post-hemiplegic tremor can be ex- 
cluded by the history of preceding paralysis and the increased reflexes. 
Hysteria must be considered. 

Treatment. — Medication appears to be of no avail. Massage, elec- 
tricity and vibration have been of service. The administration of ex- 
tracts of the parathyroid glands has been advised. 

ACUTE CHOREA 
(Chorea Minor. Sydenham's Chorea. St. Vitus' Dance) 

Definition. — A nervous affection, common in children, characterized 
by irregular involuntary muscular contractions, resulting in purpose- 
less movements, and often accompanied by psychic disturbances. 

Etiology. — The disease is common between the ages of five and fif- 
teen, especially in girls. A neurotic heredity can often be traced. The 
strain of school-life is usually the chief factor. Sudden fright or ex- 



552 



FUNCTIONAL NERVOUS DISEASES 



citement often precedes the appearance of symptoms. About 25% of 
the patients gi\e a historj^ of antecedent rheumatism. Any acute in- 
fectious disease or other condition lowering the vitality of a child may 
be an accessorj^ cause of chorea. 

Morbid Anatomy. — Death from chorea is rare and pathological 
studies relatively few. Minute emboli in the cerebral vessels have been 
found in some cases, and have led to the theory that chorea is caused 
by numbers of such emboli taking their origin from a rheumatic endo- 
carditis. This theory covers but a part of the cases. 

Perivascular hemorrhages and areas of infiltration in the brain have 
also been observed. The pathology is by no means established. 

Bacteria. — Many investigators have found bacteria in the brain, 
but the organisms have been of wide variety, usually streptococci. 
Poynton and Paine found their streptococcus rheumaticus in the cere- 
bral embolisms. The dependence of the disease upon bacterial infec- 
tion is not established, but the theory that it is due to the action of 
toxins, probably bacterial, upon a sensitive nervous system receives much 
support. 

Symptoms. — Motor.- — Irregular, jerky, purposeless movements of 
one or both upper extremities are first noted. The movements may be 
confined to one extremity or extend to all. The face may be affected. 
With these movements awkwardness and weakness in the use of the 
hands or other parts develop. The patient drops things because of the 
chorea and is often rebuked or punished for carelessness. Speech may 
become hesitating, jerky and imperfect. The movements may be \ery 
slight, occurring at rare intervals and for some time scarcely attract- 
ing attention. In the mild form they cease during sleep. They are 
regularly increased by excitement or embarrassment, and are there- 
fore often most noticeable during examination. In severe cases the 
jerky movements affect all parts of the body, are almost constant, more 
violent, and may persist during sleep. The weakness may develop into 
paralysis. 

Psychic. — Irritability, peevishness and inability to concentrate the 
attention attend the milder cases. In severer forms the mental dis- 
turbance becomes more marked. Delirium with varied hallucinations 
may develop. Stupor and dementia have been observed in fatal cases. 
Constitutional anemia, malnutrition and loss of appetite are regularly 
present. The pulse is rapid and the patients feeble. Fever appears 
only in the severer cases. 

Complications. — Heart murmurs are common. They may be 
hemic or due to definite endocarditis. The location of the apex impulse, 
the size of the heart, the character of its action, and the circulatory 
conditions must all be considered in attempting to decide this question. 
Acute pericarditis occasionally develops. Other rheumatic complica- 
tions, such as erythema nodosum, purpura and subcutaneous nodules, 
may be seen. 

Course. — The disease runs its course in two or three weeks or 



CONVULSIONS OF CHILDREN 



553 



months. It regularly ends in recovery. Occasional choreic movements 
may be seen for months afterward. Death is possible in the severe 
forms. 

Treatment. — Freedom from disturbing influences of any kind, fresh 
air and good food are the prime requirements. The home conditions 
must be made favorable or the child removed from them. Relief from 
school duties, an out-door life, and nutritious food will prompt^ re- 
lieve mild cases. In pronounced cases rest in bed is necessary. 

Arsenic is regularly administered. Fowler's solution in doses of 
2 to 5 minims, thrice daily, is commonly given. Some increase the dose 
to the limit of intolerance, but this seems undesirable. 

Chloral and the bromides are often given for sedative effect. i\Iassage 
and passive movements may be employed. In chronic cases suggestion 
and educative exercises are of value. 

CONVULSIONS OF CHILDREN 
(Infantile Convulsions) 

Definition. — General tonic and clonic convulsions occurring in child- 
hood from various causes, not including epilepsy. 

Etiology. — A familj^ tendency to nervous disturbance is notable in 
some cases ; in others the individual seems to have an abnormally sensi- 
tive nervous system. The origin of this Aveakness can often not be 
made out. In children of such hereditary or acquired nervous suscep- 
tibility any form of trauma, toxemia or infection may be the cause of 
a general convulsion. The possible causes of convulsions in childhood, 
therefore, include practically all the varied forms of disease or injury 
to which they are subject. Certain influences are so important as to be 
specially enumerated. 1. Gastro-intestinal disorders of any kind, espe- 
cially overloading the stomach with indigestible food, and constipation, 
are the commonest causes of convulsions in childhood. Intestinal para- 
sites and inflammations of any kind are important factors. 

Dentition is commonly regarded as the most frequent cause of in- 
fantile convulsions. In most instances it is some associated alimentary 
disorder and not the "cutting of the teeth" that causes the disturb- 
ance, yet in very sensitive children "teething" alone may cause con- 
vulsions. 

2. In childhood the invasion of an acute infectious disease, espe- 
cially pneumonia, scarlet fever, whooping-cough or small-pox, is fre- 
quently marked by a convulsion. The initial chill commonly seen in 
adults at the onset of such acute infections seems to be replaced in 
childhood by a convulsion. 

3. Rachitis predisposes children to convulsive seizures. 

4. Any illness or indisposition lowering the vitality of a child favors 
these convulsive seizures. 

5. Fright or excitement may precipitate a convulsion in a suscepti- 
ble child. 



» 



554 FUNCTIONAL NERVOUS DISEASES 

Symptoms. — The convulsions may occur in a child apparently in 
perfect health or they may be preceded by irritability and restlessness 
with evidences of digestive disturbance. 

The seizures vary from attacks of brief unconsciousness Avith little 
or no spasm to general tonic and clonic convulsions not to be distin- 
guished from the characteristic fits of epilepsy. 

In the milder attacks, the so-called "inward spasm," the child be- 
comes silent, rigid, stares or rolls the eyes upward, the face or one hand 
twitches for a moment and the paroxysm is over. 

The severer paroxysms begin in like manner, but the whole body 
becomes rigid, the hands clinched, the elbows flexed, the head retracted, 
and quick spasmodic jerkings of the face and extremities follow. The 
respiration is embarrassed, the pulse becomes rapid, feeble, and possibly 
imperceptible. The face and lips become deeply cyanosed and death 
appears imminent. There may be frothing at the mouth and rattling 
of mucus in the throat. After lasting a few seconds or several minutes 
the convulsion gradually ceases, the muscles relax, and the child passes 
into a stupor from which it rouses slowly, perhaps hours afterward. 
The attacks may be repeated at any time ; frequently several follow one 
another at short intervals, and many may occur in a day. Death rarely 
follows a single convulsion, but may result if the convulsions are fre- 
quently repeated. 

The convulsions are likely to recur, but may not. In most cases they 
cease entirely as the child grows older. Persistence of the convulsions 
usually means epilepsy. 

Diagnosis. — The convulsion can be recognized on sight or history. 
The cause is the important question and must be sought with care. A 
thorough physical examination and a study of the diet and life of the 
child should be made to determine the conditions which have caused 
the convulsions. Epilepsy can be excluded only after prolonged ob- 
servations, but it is to be remembered that convulsions are common, 
epilepsy in infancy relatively rare. 

Treatment. — During the convulsion chloroform should be given by 
inhalation. If the tongue is protruded or caught between the teeth a 
bit of wood or rubber should be used as a gag to prevent injury to it. 
A hot bath or hot pack, w^th mustard added to the Avater in the propor- 
tion of a tablespoonful to the gallon, should be given at once with the 
object of reducing internal congestion by bringing the blood to the 
surface. The bowel should be emptied by an enema, and castor oil given 
by mouth. Chloral and the bromide of soda may then be given by 
rectum, 5 grains of chloral and 10 of the bromide to a child of a year 
or more. If the danger of recurrence seems great, morphine sulphate, 
gr. 1/50 for a child of one year, may be given hypodermatically. 

Quiet and a restricted diet should be required for several days be- 
fore allowing return to the ordinary mode of life. Careful examina- 
tion should then be made for any possible cause of convulsions. The 
diet and regulation of the life are of prime importance. Rachitis if 



EPILEPSY 



555 



present must be treated. Adenoids may require removal. Anemia 
should be treated, and in every way the general health of the child 
maintained at the highest point. Excitement or excess of any kind 
must be avoided. If under such care convulsions are repeated the prob- 
ability of epilepsy is increased. 

EPILEPSY 

Definition. — A nervous affection characterized by periodic attacks 
of unconsciousness commonly associated with general convulsions and 
frequently preceded by an aura. 

Etiology. — Epilepsy regularly develops in childhood in either sex, 
and rarely begins after the age of thirty. Heredity plays an important 
part. If epilepsy itself is not present in the family, neuroses of some 
kind are often found. 

Syphilis, tuberculosis or alcoholism in the parents predisposes to 
epilepsy. Every influence which lowers the nervous vigor of a family 
favors the development of epilepsy. Similarly any influence which 
lowers the nervous vigor of the individual may in a susceptible person 
precipitate the first attack or cause the repetition of the convulsions, 
(a) Toxic influences, such as alcohol, tobacco, or the toxemia resulting 
from overburdening the alimentary tract and constipation, are of 'first 
importance, (b) Acute disease of any kind, especially the acute in- 
fectious diseases, may precede the onset, (c) Reflex irritations from 
eye-strain, adenoids, intestinal parasites, uterine or ovarian disease, 
phimosis and the like, (d) Mental shock or excitement are important 
agencies, (e) In females the attacks are likely to occur at the time of 
menstruation. 

The cerebral hemorrhages of birth, injuries to the skull at that time 
or later, defective cerebral development from any cause, all favor 
epilepsy. Idiocy or imbecility and epilepsy are frequently associated. 

Morbid Anatomy. — Many brain lesions have been found in patients 
suffering from epilepsy, especially defects of development, poren- 
cephalus, hemorrhage, cysts, tumors, meningitis and the like. These 
lesions are not essential, however, but may be regarded as sources of 
irritation which favor the development of convulsions. Recently care- 
ful studies have shown that in those dying of epilepsy degenerations in 
the cerebral nerve-cells, especially those of the second cortical layer, 
can be demonstrated. These degenerations involve especially the nuc- 
leus and nucleolus. 

Epilepsy is still, however, regarded as a functional disease — i.e., 
without definite anatomical basis. 

Symptoms. — 1. Grand Mal. — The seizures of general convulsions 
are the typical form of the malady. These include a tonic stage, a clonic 
stage, and a period of stupor or coma, and in many cases are preceded 
by an aura. 

The Aura. — A warning of some kind occurs in many cases ; it may be 
motor, sensory or psychic. Motor, A tremor, a jerk or movement of 



556 



FUNCTIONAL NERVOUS DISEASES 



some part or parts of the body, rapid revolution, or ninning forward 
a few steps are sometimes seen. Sensory aur^e are more common. 
Tingling, burning, numbness, a certain sound, a flash of light and various 
other unusual sensations are recorded. Psychic auras present them- 
selves as a certain mental depression or exaltation, certain emotions, 
or recollections. AA^hatever the aura it is repeated, as a rule, before 
each fit. The aura may just precede the paroxysm, but sometimes an 
interval of some minutes elapses before the onset. Aurae are present in 
a majority of patients but not in all. 

Tonic Stage. — The patient suddenly becomes unconscious and falls, 
often injuring himself about the head and face in falling. The whole 
body becomes rigid. The head is drawn back or to one side, the eyes 
are turned upward and to one side, the face is pale, the thorax immov- 
able (apnea), the limbs flexed. Often the sudden contraction of the 
respiratory muscles causes an inarticulate cry. The tonic stage lasts 
but a minute or two. 

Clonic Stage. — The convulsive movements begin in the face- or an 
extremity, but quickly become general. The eyes, face, limbs and whole 
body are thro^^na into violent jerky contractions, the teeth are ground 
together, the tongue is protruded and often bitten, the saliva is churned 
into froth and pours from the mouth, the respiration is jerky and im- 
perfect, the face becomes cyanotic, the pulse rapid and weak. The 
contractions last from one to five minutes, and then gradually die out. 
Both bladder and rectum are commonly evacuated during the paroxysm. 
Stupor or complete coma follows, lasting a half hour or more. The 
patient then awakes, possibly unconscious that he has had a convulsion, 
but usually weak, depressed and mentally confused. 

Recurrence. — Epileptic fits recur after varying intervals, hours, days, 
months or years. The fits often occur in groups. Fright, fatigue, ex- 
citement and the like may precipitate an attack, but usually they recur 
without apparent cause. In most cases the attacks slowly increase in 
frequency. 

Nocturnal epilepsy is common, the fits coming on at any time dur- 
ing the night, even in sleep. Under these circumstances the patient may 
not know what has happened or may be aware from the muscular sore- 
ness, exhaustion or the bitten tongue that he has had a fit. 

Status Epilepticus. — In some instances, especially late in the dis- 
ease, the fits are repeated in a long series, are accompanied by fever, 
even 104° to 105° F., and followed by collapse. Such crises end favor- 
ably, as a rule, but death may occur. 

Postepileptic State. — Usually the mind quickly clears, but it may re- 
main clouded. A trance-like condition may supervene, and mania with 
homicidal tendencies is well known to follow in some cases. 

2. Petit Mal. — Temporary unconsciousness with few or no convul- 
sive signs marks this condition. The manifestations are varied. In some 
a sudden pallor, a fixed stare, a momentary obliviousness, are all that 
are seen. Slight tremor of the eyes, face or an extremity may be seen. 



EPILEPSY 



557 



The patient may fall or may drop what he is holding. The urine may 
be passed involuntarily. 

In other cases the patient turns rapidly about, or runs a few steps 
in an automatic manner, and then returns to his usual condition. 

Psychic Equivalents. — In rare cases the epileptic seizure is replaced 
by some unconscious and automatic act. Murder has been done, and 
tires set by the irresponsible victims of such seizures. In other cases 
long journeys have been taken or various complicated acts performed. 
Ordinary convulsions occurring before or after such paroxysms reveal 
their nature. 

Course. — The disease tends to grow worse with steady increase in 
frequency of the convulsions and increasing mental dulness in the in- 
tervals. The patients may die from their falls or injuries received 
while unconscious (drowning) or from the convulsions, or in a condi- 
tion of dementia. 

Diagnosis.— The typical fit can hardly be mistaken. The aura, tonic 
and clonic spasm and subsequent stupor are very characteristic. Repe- 
tition of the convulsions is highly suggestive. The presence of scars 
or bruises on the scalp or the tongue is helpful. Nocturnal fits are regu- 
larly epileptic. In children under two years convulsions are often re- 
peated a number of times and then cease, without subsequent epilepsy. 
The family history is important, but time is required to settle the ques- 
tion. In adults the convulsions of uremia are sometimes mistaken for 
epilepsy. The anemia, cardiac changes, arteriosclerosis and urinary 
findings should differentiate the condition. 

Hysteria is easily recognized. The fit is overdone. The patient is 
noisy, never injures himself or herself, but may strike others ; the con- 
vulsion is exaggerated, unconsciousness is feigned, but there is no 
relaxation of the sphincters and no coma. 

3. Jacksonian Epilepsy. — (Cortical, symptomatic or partial epi- 
lepsy.) In this condition the seizures are limited to one extremity or 
to one side of the face. The convulsion may extend from one part to 
another, as from the arm to the leg or vice versa. The localized form 
may at any time give place to a general convulsion. Jacksonian epi- 
lepsy usually arises from focal irritation of the brain, such as a de- 
pressed fracture, a localized meningitis, a tumor or abscess. Similar 
attacks may occur in uremia. The location of the focal lesion is usually 
indicated by the part in which the convulsion begins. 

Prognosis. — Some few patients recover, but the disease is generally 
incurable and tends to be progressive. 

Treatment. — General. — The patient must be examined thoroughly 
for any defect which may be a source of irritation. Eye-strain, aden- 
oids, uterine displacement, any possible source of local irritation should 
be relieved. The digestion should be studied, an easily digestible diet 
prescribed, and constipaticm avoided. An out-door life with freedom 
from annoyance or care is helpful. IModerate exercise is desirable. 
Excess of any kind must be forbidden. 



558 



FUNCTIONAL NERVOUS DISEASES 



Medicinal. — Bromide of potassium or sodium is effective in reduc- 
ing the frequency of the paroxysms. Small doses, 5 grains, are given, 
and the dose later increased. If acne appears, the medicine must be 
reduced or stopped. It may be continued indefinitely. Many other 
nerve sedatives, chloral, cannabis indica, zinc, etc., are employed. 

Institutional. — Control of the mode of life of the epileptic patient 
is essential. If this cannot be secured at home, removal to a sanatorium 
should be urged. Great numbers of epileptic patients are now treated 
advantageously in farm-colonies, such as the Craig Colony, Sonyea, 
N. Y. Jacksonian epilepsy may be relieved by trephining and appro- 
priate treatment of the focal lesion. 

MIGRAINE 
(Megrim. Sick Headache) 

Definition. — An affection characterized by attacks of severe head- 
ache, often attended by disturbances of vision and digestion. Migraine 
presents a close analogy to an epilepsy in which the motor discharges 
are replaced in large part by sensory phenomena. 

Etiology. — The explanation of migraine is regularly based on two 
factors, a constitutional nervous defect or weakness, and some local dis- 
turbance or weakness, (a) Constitutional. Heredity is regarded as 
important. Some neuropathic taint (headaches, epilepsy, neurasthenia 
and the like) can usually be found in the family. A gouty tendency is 
sometimes present and excess of uric acid in the blood or deficiency of 
it in the secretions is commonly invoked as explaining the attacks of 
megrim. Exact proof of the relation of either of these conditions to 
megrim is, however, lacking, and the common accusation of uric acid 
in this regard is without adequate foundation. 

(b) Local conditions. These comprise most functional and organic 
defects, such as simple constipation, eye-strain, adenoids, nasal spurs 
and polypi, uterine or ovarian disease and the like. In general any 
influence which lowers the health of the patient or acts as a source of 
local irritation may have relation to attacks of migraine. In many cases 
it is quite impossible to determine the etiology. The affection appears 
in families without neuropathic taint and in healthy individuals. The 
attacks begin in childhood or early adult life, more often in females. 

Symptoms. — Prodromal disturbances announce to some the ap- 
proaching attack. The prodromata are varied, languor, drowsiness, 
flashes ot light, spasm of ocular muscles, dilatation of the pupil and the 
like. The headache itself usually begins in the morning. The pain is 
referred to any part of the head, usually unilateral, sometimes sharply 
localized. Visual disturbances commonly accompan}^ the pain. The 
sight is blurred, or there may be definite hemianopsia. 

In some cases varied figures with flashing colors play before the 
eyes. Nausea and vomiting are common ; the vomitus is yellow from 
the presence of bile. Vomiting is severe in some persons and may give 
relief. 



NEURALGIA 



559 



Tingling and numbness may be felt in the face or arm, and may 
be accompanied by weakness or actual loss of power. Speech may be 
slow and stumbling and temporary aphasia may develop. The face is 
usually pale from vasomotor constriction, and later the face and ear 
on the affected side may flush. The patient is greatly prostrated and 
hypersensitive to noise or disturbance of any kind. The attack usually 
lasts throughout the day or several days. The patient is prostrated for 
some time afterward. 

Course. — The attacks occur at intervals of days or weeks, sometimes 
from definite indiscretions in diet or life, but often without apparent 
reason and despite the best of treatment. They tend to become less fre- 
quent and less severe in later life. The menopause seems to bring relief 
to women. Many patients having sought relief in vain finally resign 
themselves to their suffering, and yet are able to live lives of activity 
and usefulness. 

Treatment. — The Attack. — A brisk saline cathartic taken at the 
first signal of the attack is advisable. Washing out the stomach with 
hot Avater is recommended in those cases where vomiting is severe. 
Black coffee given at the onset is sometimes helpful. During the attack 
the patient must be kept in bed and heat applied to the feet. Acetanilid, 
phenacetin and caffeine are given for relief of the pain, and are some- 
times helpful, if they can be retained. Morphine may be required for 
the very severe attacks, but should be withheld, if possible. Often the 
after-effects of morphine are so disagreeable to these patients that its re- 
lief is declined. Hot or cold applications, as preferred, may be made to 
the head. 

General. — In the intervals the life of the patient should be carefully 
planned. A vegetarian diet helps some, but dietary restrictions are 
usually valueless. Avoidance of such articles of food as cause gastric 
disturbance usually commends itself to the patient. Excesses of any 
kind should be avoided. Abundance of sleep and rest is advisable. An 
out-door life and moderate exercise are recommended. 

Local. — Every defect should, if possible, be corrected. Thus errors 
of refraction, adenoids, bad teeth, digestive disturbances, especially con- 
stipation, uterine or ovarian disease and the like must be appropriately 
treated. 

NEURALGIA 

Definition. — A painful affection of a nerve or nerves without dis- 
coverable lesions either in the nerve itself or adjacent tissues to ex- 
plain it. 

The term is a broad one which commonly is loosely used to cover all 
types of pain. Every effort should be made to distinguish neuralgia, on 
the one hand, from pain excited by definite nerve changes such as occur 
in neuritis, and on the other from pain due to definite local lesions, such 
as abscesses, new growths and the like. Even with the most careful 
study, however, we may be unable in some cases to distinguish neuralgia 
from neuritis. 



560 



FUNCTIONAL NERVOUS DISEASES 



Etiology. — The affection is rarely met with in childhood, but is com- 
mon among adults, especially women. A neurotic tendency or heredity 
underlies many cases. The weak and anemic are most subject to it. 
Constitutional conditions producing weakness and anemia may precede 
it, especially infectious diseases, such as influenza and malaria, or the 
systemic poisons of rheumatism, gout, diabetes or chronic nephritis, or 
alcohol, lead or arsenic. In those liable to the affection, exposure to 
cold and wet, or any condition producing nervous exhaustion or debility 
may precipitate an attack. In not a few cases no cause can be found 
and we must be satisfied to call them idiopathic. The term ought not 
to be applied to pains which can be explained by definite pathological 
lesions, such as caries of the teeth, suppuration in the antrum of High- 
more, pressure of tumors and the like. The more carefully patients are 
studied the less use we shall have for this designation. 

Symptoms. — Neuralgia presents itself in the form of paroxysms of 
pain, usually described as sharp, burning or stabbing, in the territory 
of a certain nerve or nerves of one side of the head or body. The 
paroxysms last for a brief time or may be protracted. In the intervals 
there is usually no discomfort. The pain is usually severe, and may be 
agonizing. Regularly there are no changes seen in the affected area. 
There may, however, be vasomotor or finally trophic changes in per- 
sistent cases. Thus the skin may be hot and red, or cold and pale. 
Edema, atrophy or induration of the skin, or whitening of the hair in 
chronic cases may be seen. Where herpes or such changes as these are 
met with we are probably dealing with manifestations of definite lesions 
of the nervous system. (See Herpes Zoster.) 

The attacks of pain are likely to recur at regular intervals of a day 
or days, without relation to malaria. The pain often shifts from one 
nerve to another. Along the course of the affected nerve there may be 
tender points, especially where it emerges from a canal or becomes more 
superficial. The affection lasts for varying periods, weeks or months, 
or in some cases persists for life. Any nerve in the body may be affected. 
The more important varieties follow: 

(1) Trigeminal Neuralgia. Tic Douloureux. Any of the branches 
of the fifth nerve may be involved. The attacks of pain are character- 
istic. The affection is often severe and protracted, and may require 
heroic measures for relief. Before accepting the diagnosis of neuralgia 
we must carefully exclude organic lesions, such as the pressure of tumors, 
cerebral or in the course of the nerve, disease of bone causing pressure 
in the course of the nerve, or any cause of peripheral irritation, such as 
caries of the teeth, suppuration of the antiiim or the frontal or etlmioidal 
sinuses, or the growth of tumors within the orbit, nose or mouth. In 
neuralgias of the ophthalmic division the possibility of glaucoma, or 
errors of refraction or muscular defects of the eyes must be considered. 

(2) Intercostal Neuralgia. — This is frequently a severe type of 
the affection. Care must be taken to exclude pressure on the nerve by 
diseased vertebrae (Pott's disease) or aneurisms or other tumors. Pleurisy 



CHRONIC ULCERATIVE PHTHISIS 



401 



ing of the normal side for pathological. Much less frequently the breath 
sounds may be harsh or broncho-vesicular. Often the respiratory mur- 
mur is interrupted or wavy (cog-wheel breathing). The voice sounds 
usually show no appreciable change. A few fine rales are frequently 
heard over the affected area and are of much significance. They may 
be due to the localized bronchitis, to the pleurisy or to beginning soften- 
ing. A short, sharp cough followed by a quiet inspiration will often 
disclose the presence of rales not heard under ordinary conditions. For 
their detection and localization the stethoscope is to be preferred to the 
unaided ear. 

Signs of the Advanced Stage. — Inspection shows emaciation of vary- 
ing degree, anemia, increase in breathing rate, pronounced retraction 
above and below the clavicles, restricted chest expansion and often a 
much increased area of cardiac pulsation. Palpation verifies the restric- 
tion of chest movement and reveals increased vocal fremitus over 
areas of consolidation or diminished fremitus over thickened pleura or 
pleuritic effusion. Friction fremitus, or that corresponding to coarse 
rales or rhonchi, may also be felt. Percussion gives dulness of varying 
degrees, corresponding to the extent and completeness of the consolida- 
tion. It also often shows immobility of the lung borders, especially over 
the liver and heart, which indicates pleuritic adhesions. A large and 
superficial cavity may give a tympanitic or amphoric note or the cracked- 
pot sound. Usually, however, the cavities are so surrounded by consoli- 
dation, or are so filled with secretion, that they give no characteristic 
percussion note. Over areas of complete consolidation auscultation 
shows tubular (bronchial) breathing and bronchophony. In other places 
the breathing may be broncho-vesicular ; in still others it may be greatly 
diminished, because of fibrosis or from pleuritic adhesions. Rales are 
usually abundant and may be of all possible varieties, from the fine 
crepitant rales of hepatization to the loud, coarse, gurgling sounds of 
a cavity containing secretion. 

A cavity does not often show characteristic signs. This may be due 
to its small size ; to its being deep in the lung, or surrounded by consoli- 
dation, or filled with secretion, or to the fact that its communication with 
a bronchus is not free. Usually, however, the breathing over it possesses 
the exaggerated, hollow, tubular quality known as cavernous. If this 
has beside a musical quality it is called amphoric. The voice also 
has the same cavernous character and the whisper is heard with astonish- 
ing distinctness and loudness — as though through a trumpet (whispering 
pectoriloquy). The characteristic rales of a cavity are very coarse, 
loud, gurgling sounds which have a peculiar resonant quality. Palpa- 
tion may reveal absence, diminution or increase of the vocal fremitus, 
or the crepitation of coarse rales. 

Complications. — Pleurisy with effusion is common. The fluid may 
be serous, hemorrhagic or, rarely, purulent. 

Pneumothorax occurs occasionally — usually by the perforation of a 
small, superficial cavity. Tuberculosis of the larynx, and of the intes- 
26 



402 



THE INFECTIOUS DISEASES 



tines, develops at some time in about half of all eases. The disease may 
attack the meninges, brain, peritoneum, pericardium, kidneys, bladder, 
liver, etc. Compensatory emphysema is very common in the unaffected 
portions of the lungs. Lobar pneumonia or pulmonary gangrene may 
occur. Other complications are fistula in ano, dilation of the stomach, 
venous thrombosis and endocarditis. Although actual endocarditis is 
comparatively rare, heart murmurs are by no means uncommon. They 
are systolic in time and are located either at the apex or over the pul- 
monic area. Retraction of the lungs from fibrosis often causes great 
increase in area of cardiac pulsation and sometimes actual displacement 
of the heart. 

Diagnosis. — The importance of a diagnosis at the earliest possible 
moment cannot be overestimated. The historj^ of the case, the symptoms, 
and the physical signs should be carefully studied and weighed. The 
sputum should be examined, repeatedly, if necessary, for tubercle bacilli, 
the presence of which furnishes the only absolute proof of the disease. 
Failure to find the bacilli does not prove conclusively the absence of 
tuberculosis. The presence of elastic fibers in the sputum is evidence of 
the destruction of lung tissue, but these are found in other conditions 
than tuberculosis — e.g., pulmonary gangrene. 

Other Diagnostic Aids. — I. Tuherculin. — A variety of prepara- 
tions derived from tubercle bacilli are now used under the name of tuber- 
culin. The best known and most commonly employed of these is that 
first prepared by Koch and now known as old tuberculin or T.O. This 
tuberculin is prepared by growing cultures of the tubercle bacillus on 
glycerine-beef -broth for 6 to 8 weeks, sterilizing the cultures by heat, filter- 
ing out the dead bodies of the bacilli, and finally evaporating the filtered 
* fluid to one-tenth its original volume. For diagnostic purposes this 
tuberculin is employed in several ways. 1. On the skin, (a) Moro's test. 
An ointment (Moro's ointment) is prepared by mixing equal parts by 
weight of tuberculin and lanolin. Fifteen grains (1.0 gm.) of such an 
ointment are rubbed vigorously into the skin of the abdomen over an 
area of 2 or 3 inches in diameter. As a control an equal quantity of 
lanohn alone may be rubbed into a corresponding area. A positive 
reaction consists in the development upon the first area of a papulo-ery- 
thematous eruption in from one to three days. The number of papules 
varies from one to several hundred, and the activity of the reaction 
may be estimated by their number. 

(b) Von Pirquet's reaction. For this purpose a 10 per cent, dilu- 
tion of tuberculin is employed. Two minute scarifications or linear 
scratches are made upon the forearm, at a distance of 2 or 3 inches from 
each other. Into one of these a drop or two of the diluted tuberculin 
is rubbed. The other area serves as a control. In the tuberculous indi- 
vidual the test area becomes reddened, raised, and surrounded by an 
erythematous zone of varying size. The area is distinctly indurated 
and vesicles may form upon it. The reaction fades gradually in the 
course of several days and may persist for a week or more. 



CHRONIC ULCERATIVE PHTHISIS 



403 



2. In the conjunctiva. Calmette's ophthalmic reaction. For this 
purpose a 1/2 to 1 per cent, solution of the dried alcoholic precipitate of 
old tuberculin is used. One or two drops of this solution are dropped in 
the conjunctival sac. Within twenty-four hours an active conjunctivitis 
develops in positive cases. The conjunctiva becomes swollen, reddened, 
and a watery, fibrinous or even purulent exudate appears, accom- 
panied by lachrymation. The reaction has been so severe in many cases, 
resulting in permanent damage to the eye, that it is no longer recom- 
mended. 

3. Under the skin. The subcutaneous injection of tuberculin is 
applicable only in afebrile cases. The dosage employed varies con- 
siderably in different hands. One milligram is a safe initial dose. 
If no reaction follows, a second injection of 2 milligrams may be 
given after two or three days. In case of failure after this dose larger 
doses may be tried, even up to 10 milligrams, but the smaller doses are 
usually satisfactory. To the subcutaneous injection of tuberculin 
the tuberculous patient reacts by a rise of temperature of several 
degrees, usually accompanied by more or less pain in the back and 
limbs and general malaise. A slight intensification of the physical signs 
in the chest may be noted. The reaction rarely lasts more than ^twenty- 
four hours. The subcutaneous injection of tuberculin should not be 
resorted to in very debilitated patients, nor in those with advanced disease 
of the heart, arteries, or kidneys. 

Reaction to any of the tuberculin tests is evidence that the person 
tested has a tubercular lesion in some part of his body, but not neces- 
sarily an active process. Positive reactions are, therefore, frequently 
obtained in adults suffering from other affections. In childhood such 
reactions are much less common. 

II. RoNTGEN Rays. — The Fluoroscope. — The screen enables one to 
study differences in the excursion of the diaphragm on the two sides 
due to impaired function of one lung. Inequality in the excursion is 
known as Williams' sign. 

The Skiagraph. Radiographic plates of the lungs, when well 
taken, give invaluable information as to the presence or absence of tuber- 
culosis. Undoubtedly lesions may, in some cases, be demonstrated by 
the X-rays before they are appreciable by ordinary methods of examina- 
tion. Difficulties arise from the fact that latent tuberculosis or other 
lesions may be misinterpreted. Expert training is necessary for correct 
interpretation of the plates (see Fig. 79). 

Prognosis. — The prognosis is often very uncertain and difficult. Most 
cases of chronic phthisis eventually prove fatal, but that many cases 
result in what is practically a cure is shown by the great frequency with 
which healed or latent tuberculosis is found in the lungs of old persons 
who have died from some other cause. The disease may progress steadily 
and rapidly and be fatal in from six months to a year, or it may remain 
stationary for long periods and last for ten or even twenty years. It 
tends to progress more slowly in those of middle age than in young 



404 



THE INFECTIOUS DISEASES 



persons. High fever, progressive emaciation, profuse expectoration, signs 
of extensive consolidation and softening, severe hemoptyses, laryngeal 
symptoms and persistent diarrhea are the chief unfavorable features. 

FIBROID PHTHISIS 

The term fibroid phthisis has sometimes been used to include all 
fibroid disease of the lungs whether tuberculous or not ; but it is more 
properly restricted to that form of pulmonary tuberculosis in which 




Fig. 79. — Extensive tuberculosis of the right upper lobe, which appears very dark as compared with 

the normal left apex. 

fibrosis is the predominant change and caseation and softening are slight 
or altogether lacking. It is probable that in some of the cases the 
primary process has been a simple fibrosis upon which tuberculosis has 
become engrafted. The condition is not common and is met with chiefly 
in adults. 

Morbid Anatomy. — As a rule the process begins at one apex and the 
lesion is usually confined chiefly to one lung. The lung is small, in- 
elastic, tough, and shows throughout a great increase in fibrous tissue 
diffusely scattered or in dense bands. The pleura is firmly adherent and 
is often enormously thickened. Old caseous nodules may be found at 



FIBROID PHTHISIS 



405 



the apices or in the bronchial giands. The bronchi show a chronic 
bronchitis and often also bronchiectasic cavities. In the unaffected lung 
there is compensatory emphysema. 

The clinical course is extremely chronic. Cough is usuall}^ the 
chief symptom and is especially troublesome in the morning. Expectora- 
tion is profuse and results from the chronic bronchitis or from bronchiec- 
tasis. It may be fetid. Tubercle bacilli are scanty and may be absent 
for long periods. Fever is uncommon. There may be hemoptysis or pleu- 
ritic pain. The right heart eventually dilates and weakens and adds its 
special train of symptoms, such as dyspnea, cyanosis, ascites, etc. 

The physical signs are those of other types of chronic interstitial 
pneumonia : marked sinking and retraction of the affected side of the 
chest with drooping of the shoulder; feeble or absent expansion upon 
breathing; displacement of the heart; impaired resonance or dulness; 
feeble or tubular breathing, and moist rales or rhonchi. Bronchiectasis 
may give the signs of a cavity. The tuberculous nature of the process 
may be very difficult to demonstrate since tubercle bacilli are often 
absent from the sputum. The condition lasts for many years and may 
become serious only with the advent of cardiac weakness. 

Prophylaxis. — Since the infectious matter is spread almost wholly by 
means of sputum the greatest care should be taken in properly disposing 
of this. Patients should be instructed scrupulously to avoid spitting on 
the floors of rooms, public buildings or conveyances, or even in the street. 
All sputum should be collected in spit-cups or wide-mouthed flasks con- 
taining a 5 per cent, solution of carbolic acid, or corrosive sublimate (1- 
500), or else should be received in pieces of cheesecloth or rags which 
can then be burned. If handkerchiefs are used the sputum should not 
be allowed to dry upon them and they should be thoroughly disinfected 
by boiling for one hour. This applies also to night gowns, bed linen and 
other articles which may be contaminated. If such precautions are 
faithfully observed the risk of infection to other members of the family 
is very slight indeed. The danger to young children from the use of 
milk from tuberculous cows is a real one and can be removed only by 
the careful and systematic inspection of dairies and cattle and the elim- 
ination of all animals suffering from the disease. 

The children in tuberculous families should be reared with great care, 
especial attention being given to the avoidance of catarrhal troubles of 
the upper air passages, to the removal of adenoid growths and enlarged 
tonsils, and to the maintenance of vigorous health and good digestion. 
They should live an out-of-door life, if possible, in a mild, suitable 
climate, and their diet should include an abundance of milk, eggs and 
fats. Tuberculous mothers should not nurse their infants. Persons 
suffering from pulmonary tuberculosis, in an active stage at least, should 
not marry. 

Treatment of Pulmonary Tuberculosis. — It is important to bear in 
mind that, in many cases, at least, of tuberculosis, there is a distinct ten- 
dency toward spontaneous cure, as is shown by the frequency with 



406 



THE INFECTIOUS DISEASES 



which healed tuberculosis is found at autopsy. This tendency seems 
related to the state of general nutrition and the vigor of the vital 
processes rather than to local conditions in the lungs. 

In like manner modem treatment is directed toward the building up 
of the general health and nutrition rather than to the lungs themselves. 

Treatment of the Disease.; — (a) Climate and Fresh Air. — An abun- 
dance of fresh air is the most important single remedy in the treat- 
ment of tuberculosis. Its importance, as distinguished from that of 
climate itself, has been much more generally appreciated in recent years, 
and this has led to most gratifying results. The fact that the patient 
must be treated at home and in the city should not prevent the sys- 
tematic and careful carrying out of this measure. The plan is simply 
to give the patient, both in Avinter and summer, the greatest possible 
amount of fresh air and sunshine. In the daytime, if not bedridden, he 
should spend all of his time out of doors, properly protected from cold 
and wind. If confined to bed the windows should be widely opened and 
the bed kept in the sunlight as much as possible. Whenever possible, 
he should be moved to a couch on a sunny balcony or porch, well 
wrapped up and sheltered from the wind. At night the patient should 
occupy a room by himself, with the windows wide open. Cough, fever, 
sweating, etc.^ are not contra-indications to such open-air treatment. 
This plan of treatment is much more easily carried out in a suitably 
arranged sanitorium where the patients are constantly under medical 
supervision and discipline. In Europe many such sanitoria are to be 
found, and in this country they are, fortunately, increasing in number. 
The beneficial effects of sanitorium treatment are due quite as much to 
the systematic open-air life, and the intelligent regulation of diet, cloth- 
ing, rest, exercise, etc., as to the effect of the climate itself. 

Experience has shown that many varieties of climate may be suitable 
for consumptives; the essential features of all such being pure air {i.e., 
freedom from dust), an equable temperature and an abundance of sun- 
shine, so that the patient may be out of doors almost constantly. These 
requirements are usually best met in high, dry regions, but altitude in 
itself does not seem to be of primary importance. The high tablelands 
of Colorado, Arizona and New Mexico, and the regions about Davos 
and St. Moritz in Switzerland, are well-know instances of a dry, 
elevated climate. Many cases do extremely well in the cold, moderately 
elevated climate of the Adirondacks and the Catskills. If a warmer 
winter climate is desired it may be found in the comparatively dry 
regions of North Carolina, Georgia, Southern California, Algiers or 
Egypt, or in the moister climate of Florida or the Madeira or Canary 
Islands. 

As to the locality best suited for an individual case only a few general 
rules can be given. The climate must first of all be one in which the 
patient can be constantly out of doors. The colder and more elevated 
regions are, therefore, best suited to the young and comparatively robust, 
and to those who are relatively free from fever and in whom the disease 



PULMONARY TUBERCULOSIS 



407 



is neither very active nor far advanced. Older patients, those with 
pronounced emphysema or arteriosclerosis ; and those with advanced 
lesions, emaciation and continuous fever, usually thrive best in a warm 
and less elevated cUmate. Good food and proper nursing and care are 
quite as essential as a suitable climate and the good effects of climate 
may be altogether nullified if the former be lacking. 

(b) Diet. — A gain in weight is one of the most trustworthy evidences 
of improvement, and the feeding should be regulated with that aim 
in view. Patients should be given just as much simple, wholesome food 
as they can eat and digest, even though, as is frequently the case, they 
have little or no appetite. The diet should be especially rich in proteids 
and fats in the form of milk, eggs, meat, cream, butter, etc. In many 
cases the dyspeptic symptoms are prominent and troublesome and only 
the simplest foods can be tolerated. In such cases milk, koumiss, broths, 
beef juice, beef jelly and the various prepared foods are suitable and 
should be given in small and frequent feedings. The anorexia should 
be combated by having the meals as appetizing and as daintily served 
as possible and by the use of bitter tonics, etc. When there is great 
repugnance to food or when, from involvement of the larynx, swallowing 
is difficult and painful, it may be necessary to feed by means of the 
stomach tube. Moderate fever is not a contra-indication to solid food 
unless the digestion be seriously disturbed. 

(c) Hygiene. — The importance of an open-air life has been men- 
tioned. The patient's sleeping room should be large, sunny and well 
ventilated; his clothing should be warm but light; the underclothing 
of wool but not heavy. Most phthisical patients, especially among the 
lower classes, wear much too heavy underwear and thereby increase 
rather than diminish the risks of taking cold. Thick flannel " chest pro- 
tectors " are likely to do harm rather than good. The skin should be 
kept active and healthy by daily baths and rubbings. 

Rest and exercise should be carefully regulated and systematized to 
suit the individual case and the latter should always stop short of real 
fatigue. Walking is usually the most suitable form of exercise. Moderate 
and simple arm and chest exercises frequently repeated are of decided 
value. 

(d) Drugs. — There are no specifics for tuberculosis. Most of the 
drugs used act by improving the general nutrition and so increasing the 
powers of resistance. 

Cod-liver oil is often of much value, especially in children. It 
should be given in small doses (51-2) one hour after eating. It is 
sometimes not well borne, and should not be continued if it disturbs 
digestion. Olive oil or cream is a useful substitute. Creosote, which 
has had a wide popularity in recent years, seems to act chiefly by lessen- 
ing the cough and expectoration. Because of its disagreeable taste and 
its tendency to irritate the stomach it should be given after meals in 
capsules or disguised in an aromatic tincture or in whiskey. The begin- 
ning dose of one or two minims should be gradually increased to ten 



408 



THE INFECTIOUS DISEASES 



minims three times a day, unless gastric disturbance is noticed. Creosote 
carbonate has a similar effect and is less irritating. It should be given 
in somewhat larger doses. 

Arsenic, iron, malt extract and the hypophosphites are all useful 
tonics. 

(e) Specific Treatment. — The use of the tuberculin of Koch and of its 
more recent substitutes is reserved for patients without fever and in good 
general condition. A variety of preparations of the tubercle bacillus are 
now used by different authorities in the treatment of tuberculosis. Of 
these the chief are (1) Koch's original tuberculin (O.T.), a filtered gly- 
cerine extract of cultures of the bacillus, heated to destroy any living 
bacilli. (2) T.R., tuberculin residuum, obtained by mechanically crush- 
ing or dividing cultures of the bacillus, treating them with salt solu- 
tion, centrifuging and employing the precipitate or residuum, (3) B.E., 
an emulsion or vaccine prepared from cultures of the bacillus, and heated 
to 60° C. (4) B.P., bouillon fittre, is prepared by filtering bouillon cul- 
tures of the bacillus. The liquid is not heated. The dosage and method of 
using these preparations vary greatly. The principle is that of employ- 
ing a minimum dose at the outset, so as to avoid any general reaction, 
repeating the injection at intervals of several days (4 to 5 or in some 
systems 10 to 12), and rapidly increasing the dose up to the limit of 
tolerance. The initial dosage of O.T. varies from 0.00000001 to as much 
as 0.0001 gram, and the maximum from 0.1 mg. to 1 gram. For the 
details of these methods special articles such as that in Osier's Modern 
Medicine, Vol. Ill, p. 415, must be consulted. 

Treatment of Special Symptoms. — Cough. — The measures directed 
toward the relief of the disease itself are usually effective in lessening 
the cough. The routine administration of cough syrups should be avoided 
if possible, as they are apt to disturb digestion. The cough is frequently 
due to the complicating laryngitis and may be relieved by appropriate 
local treatment. Inhalations of creosote, turpentine, menthol, etc., are 
sometimes efficacious. Frequently, however, some such sedative as codeine 
(gr. Y^-Ya) or heroin (gr. YvrV^) or morphine (gr. K2-/8) is needed. 
At other times some stimulant expectorant may act best. If cavities are 
present a certain amount of coughing is necessary for their proper evacu- 
ation. 

Temperature. — Fever, unless high, requires no special treatment and 
should not be allowed to interfere with the fresh air regime. As a rule, 
patients with fever must be kept at rest, either in bed or upon a couch 
or reclining chair. If persistently high the fever may be controlled 
somewhat by frequent cool spongings or by small doses of antifebrin or 
phenacetin. 

Night-sweats may often be controlled by giving an alcohol sponge 
bath at bedtime and by keeping the sleeping-room cool and the covering' 
light. If drugs are needed, atropin (gr. Yuo-Yso) is the most satis- 
factory. Other drugs used are aromatic sulphur acid (m. xx), agari- 
cin (gr. Ko-M)' picrotoxin (gr. Yeo) J^i^^l camphoric acid (gr. xx). 



TUBERCULOSIS OF CIRCULATORY SYSTEM 409 



Hemoptysis. — Absolute quiet in bed and morphine subcutaneously to 
control the coughing are the measures of chief importance. An ice bag 
may be placed over the affected region of the chest. Thrombus forma- 
tion is favored by a lowering of the general blood pressure and this is 
best accomplished by a low diet, by purging and by repeated small 
doses of aconite or nitroglycerin. The use of ergot, adrenalin, tannic 
acid, etc., is irrational and should be avoided. 

Pleuritic pain, which is sometimes very troublesome, is best treated 
by some form of counter-irritation, such as tincture of iodine, mustard 
pastes or the actual cautery. 

V. TUBERCULOSIS OF THE CIRCULATORY SYSTEM 

Tuberculosis of the heart and blood-vessels is rare at best, and is 
probably never primary. In the myocardium a few scattered miliary 
tubercles are occasionally seen, and, very rarely, also larger caseous areas. 
A few cases of tuberculous endocarditis have been recorded. Tubercu- 
losis of the aorta and the larger arteries is extraordinarily rare. On the 
other hand, the extension of a tuberculous process in the lungs or lymph- 
nodes to the walls of adjacent small veins or arteries is not uncommon, 
and this seems to be the usual way in which distribution of the bacilli 
occurs. Tuberculosis of the pericardium is described with that of the 
other serous membranes. 

VI. TUBERCULOSIS OF THE LYMPH-GLANDS 
(Scrofula) 

Positive proof of the unity of scrofula and tuberculosis was lacking 
until the demonstration by Koch of the tubercle bacillus in both. The 
lymph-nodes show an especial susceptibility to the action of the bacilli 
and in children scrofula is much the commonest form of tuberculosis. 
Even in adults the lymph-nodes are frequently invaded and the condi- 
tion is sometimes met with in advanced life. In children the disease is 
most common in those living in the dark, crowded and poorly ventilated 
homes of the poor and in asylums. Negroes seem especially prone to this 
form of tuberculosis. The frequence of bovine bacilli is notable (see 
p. 387). 

Morbid Anatomy. — The anatomical changes are similar to those 
found in other forms of tuberculosis ; miliary tubercles, caseation, soften- 
ing, sclerosis, and calcification occurring in varying combinations and 
proportions. Usually the process is a slow and relatively benign one. 

Clinical Types. — Several types are distinguished, depending upon 
the particular group of nodes involved : 

(a) CERVICAL. — This is a very common type in children. Infection 
occurs in most cases through the mouth, nose or pharynx. The tonsils, 
especially, are now regarded as important portals of entry. The pas- 
sage of the bacilli through the mucous membrane is doubtless much 
favored by catarrhal inflammation or other changes. 



410 



THE INFECTIOUS DISEASES 



One after another of the cervical nodes becomes enlarged until the 
whole chain on both sides of the neck may be involved. The process is 
usually very slow and the nodes remain for a long time firm, painless 
and separate. Eventually in most cases, they fuse into large masses 
and not infrequently undergo suppuration. When this happens the skin 
overlying the mass becomes red and adherent and the abscess may rup- 
ture externally. 

(b) Bronchial. — The lymph-nodes at the roots of the lungs are con- 
stantly involved in pulmonary tuberculosis. They may also become 
infected by extension of the process from the cervical nodes and also, 
it is believed, by the passage of bacilli through the bronchial mucous 
membrane even when no pulmonary tuberculosis exists. In some cases 
infection of the lungs seems to have been secondary to the tuberculous 
changes in these nodes. In children tuberculosis of the bronchial lymph- 
nodes is the most constant and not infrequently the only lesion found at 
autopsy. It appears to be the primary lesion in the great majority of 
the cases of tubercular infection in children in this countr^^ and from 
it many of the cases of acute general miliary tuberculosis originate. 
Although the nodes often form large tumor masses serious compression 
of the neighboring structures is uncommon. Rarely such caseous and 
softened glands have been known to perforate a bronchus, the trachea, 
the esophagus, the pulmonary artery and even the aorta. 

(c) Mesenteric (TxYbes mesenterica) . — Tuberculosis of the mesen- 
teric and retroperitoneal nodes is especially frequent in young children. 
Infection occurs regularly through the intestines, in many cases by 
means of contaminated milk. The intestine may be, but frequently is 
not, itself the seat of tuberculous lesions. The condition is not uncom- 
mon in pulmonary tuberculosis and is then usually due to the swallowing 
of sputum. The diseased nodes often form large tumor masses which 
may sometimes be felt through the abdominal wall. In children the 
symptoms are chiefly those of progressive emaciation and anemia. The 
abdomen is distended and there is usually persistent diarrhea. In many 
of the cases there is an associated tuberculous peritonitis. The disease 
is usually fatal. 

(d) General Tuberculous Adenitis. — An uncommon form of tuber- 
culous adenitis is that in which there is a general enlargement of the 
lymph-nodes all over the body. It is usually associated with moderate 
fever and with progressive wasting. The condition may closely simulate 
Hodgkin's disease. 

VII. TUBERCULOSIS OF THE SEROUS MEMBRANES 

Tuberculosis of the Pleura. — Tuberculous pleurisy is commonly sec- 
ondary to tuberculosis of the lungs or of the bronchial nodes. It may 
appear in connection with tuberculosis of other serous membranes, e.g., 
the pericardium and peritoneum, or it may be a primary condition. It has 
come to be realized in recent years that many, if not most, of the cases 
of so-called idiopathic or simple pleurisy are really tuberculous in nature. 



TUBERCULOSIS OF SEROUS MEMBRANES 411 



The disease appears in acute, subacute and chronic forms, and the 
character of the exudate may be fibrinous, serous, hemorrhagic or puru- 
lent. Frequently the serous effusion has a distinct greenish tinge. An 
occasional and very chronic form is that associated with the active pro- 
liferation of new connective tissue ; adhesion of the two layers, and the 
conversion of the pleura into a dense mass of fibrous tissue w^hich may 
be an inch or more in thickness. 

The symptoms and physical signs of tuberculous pleurisy do not 
differ from those of other forms of pleurisy. (See pages 42-56.) 

Diagnosis. — Positive evidence of the tuberculous nature of a given 
pleurisy is sometimes very difficult to obtain. If tuberculosis can be 
demonstrated in the lungs or elsewhere there is little doubt as to the 
nature of the pleurisy. If the effusion be hemorrhagic the probability 
is that the inflammation is either tuberculous or cancerous. Acute idi- 
opathic serous pleurisy is tuberculous in the majority of cases. Tubercle 
bacilh are present in the exudate (either serous or purulent) only in 
very small numbers and are difficult to find by the ordinary procedures. 
The tuberculous nature of a serous effusion can often be proven by the 
injection of several cubic centimetres into the peritoneum of a guinea 
pig. A marked preponderance of lymphocytes in the cells of the 
exudate is suggestive of tuberculosis. The von Pirquet reaction is also 
of some value, and the patients may, if necessary, be tested by tuber- 
culin injections after the fever has subsided. (See page 47.) 

Tuberculosis of the Pericardium. — This somewhat rare disease is 
usually secondary to tuberculosis of the lungs, or the bronchial and 
mediastinal lymph-nodes, or is associated with tuberculosis of the 
other serous membranes. The lesion may be that of an acute or sub- 
acute inflammation with a predominance of fibrinous or of serous exu- 
date, or may be a chronic proliferative process with adhesions of the 
two layers and complete or partial obliteration of the pericardial sac. 

The signs and symptoms do not differ from those of non-tuberculous 
types of pericarditis. 

Tuberculosis of the Peritoneum. — Etiology. — The peritoneum is 
regularly involved in acute general miliary tuberculosis and in that form 
of tuberculosis which attacks several of the serous membranes. Usually 
tuberculosis of the peritoneum is secondary to that of the lungs, in- 
testines, mesenteric nodes. Fallopian tubes, bladder or epididymis. The 
disease is most common in children and young adults, but may be met 
with at any age. It is more frequent in females than in males. Cirrhosis 
of the liver, ovarian cysts and hernia seem distinctly to predispose to 
the disease. 

Morbid Anatomy. — Both the lesions and symptoms present many 
variations. There may be an acute and extensive eruption of miliary 
tubercles over the parietal and visceral peritoneum ; and associated with 
this an exudative inflammation with the formation of a varying amount 
of serofibrinous or hemorrhagic exudate. In its more chronic form 
the disease presents two types of lesions. In one there is the develop- 



412 



THE INFECTIOUS DISEASES 



ment of large tuberculous nodules which tend to caseate, soften, undergo 
suppuration and sometimes to perforate the intestines. Sacculated col- 
lections of pus are not uncommon. In other cases the chief change is a 
fibrous overgrowth, with great thickening and retraction of the omentum 
and mesentery, and sometimes with enormous thickening of the peri- 
toneal coat of the intestines. 

Symptoms. — In the acute cases there are continued fever, abdominal 
pain and tenderness, muscular rigidity, and, often, ascites. The effu- 
sion is usually serous, but may be seropurulent or hemorrhagic. If 
ascites is lacking and tympanites and diarrhea present the symptoms 
may closely resemble typhoid fever. The chronic cases present a very 
variable clinical picture. Often the only symptoms are progressive loss 
of flesh, a slight, irregular temperature, and a retracted, rigid and some- 
what tender abdomen. A subnormal temperature is not uncommon. In 
many cases one or more tumor masses can be felt. The masses may be 
formed of the retracted and thickened omentum, of matted intestines, 
of sacculated fluid, or, rarely, of greatly enlarged mesenteric nodes. 
The most characteristic of these masses is that made by the shrunken 
omentum, which often forms a somewhat cylindrical tumor lying across 
the upper part of the abdomen. Ascites may be present in either the 
acute or the chronic type. 

Diagnosis. — The acute cases without ascites often simulate typhoid. 
The spleen, however, is usually not enlarged, the typical eruption and 
the Widal reaction are lacking and there is usually more abdominal 
tenderness and rigidity. In the chronic cases the presence of one or more 
tumor masses may lead to the diagnosis of a malignant growth or an 
ovarian cyst. Afebrile cases with ascites may be difficult to distinguish 
from cirrhosis of the liver. In all cases careful search should be made 
for evidences of tuberculosis in other parts of the body. The patient 
may be tested by tuberculin either on the skin (von Pirquet) or by 
injection (see p. 402). 

Prognosis. — Although the prognosis is, in general, bad, a considera- 
ble proportion of cases recover either spontaneously or as a result of 
operation. Cases with purulent exudation are usually fatal. The dura- 
tion of the disease varies from months to years. 

Treatment. — Every case should be given a thorough trial of treat- 
ment by such general measures as are recommended in the treatment of 
pulmonary tuberculosis. If no benefit is derived from these, laparotomy 
should be performed. Just why the simple opening of the abdomen and 
evacuation of the fluid should be so often followed by improvement or 
cure is still obscure, but the fact cannot be denied. Aspiration of the 
fluid alone has but little effect. 

General Serous Membrane Tuberculosis. — Pick's Disease — 
Chronic Polyserositis. — It happens occasionally that several serous 
membranes may be simultaneously affected, even when there is no 
evidence of a general dissemination of tubercles or of marked visceral 
lesions. The peritoneum and the pleura are the membranes most fre- 



TUBERCULOSIS OF GENITO-URINARY SYSTEM 



413 



qiiently affected, but the pericardium also may be involved. The lesions 
and symptoms do not differ from those already described under the 
separate forms of serous membrane tuberculosis. 

VIII. TUBERCULOSIS OF THE GENITO-URINARY SYSTEM 

The genito-urinary tract in both sexes is not infrequently the seat of 
tuberculous disease ; the kidneys, Fallopian tubes and testicles being the 
parts most commonly affected. 

Tuberculosis of the Kidney. — Etiology. — The kidneys are fre- 
quently involved as a part of general miliary tuberculosis, but, as a 
rule, give no distinctive symptoms. Local tuberculosis of the kidney may 
be primary, but is usually secondary to some focus elsewhere in the body, 
the infection occurring by means of the blood. Infection may, however, 
be by direct extension from the peritoneum, from carious vertebras, or 
from the bladder and ureter. The disease is much commoner in the 
male sex and is most often seen in young adult life. 

Morbid Anatomy. — The disease may be, but usually is not, confined 
to one kidney. The process seems usually to begin in the pyramids or 
calyces. Tuberculous nodules develop, undergo caseation and suppura- 
tion, and gradually invade the kidney substance so that eventually the 
organ may become riddled with cavities containing caseous material or 
pus. The pelvis also becomes involved in many cases and the ureters 
and bladder may be secondarily infected. 

Symptoms. — These often extend over many months or even years and 
show much variation in severity. There may be lumbar pain and tender- 
ness, slight or irregular fever, loss of flesh, chills, sweats, etc. Freciuent 
and urgent micturition may occur even without disease of the bladder. 
The urine usually contains pus and albumin and sometimes blood or 
fragments of cheesy matter. Careful examination will often reveal tu- 
bercle bacilli. The kidne^^ may be of normal size or may show moderate 
enlargement. 

The diagnosis from other forms of pyelitis is sometimes very difficult. 
In the absence of evidence of tuberculosis elsewhere in the body the 
positive diagnosis can be made only by the finding of tubercle bacilli 
in the urine or by the positive response to the tuberculin test. 

Treatment. — If the disease be confined to one kidney and if the 
bladder be not involved the kidney should be excised. Under other cir- 
cumstances the condition can be treated only along the general lines 
indicated in all forms of tuberculosis. 

Tuberculosis of the Bladder. — Involvement of the bladder is usually 
secondary to disease of the kidney or of the testis and prostate. The 
tuberculous nodules soon break down and form ulcers of varying extent, 
which are most common in the region of the trigone. The symptoms are 
usually those of a subacute or chronic cystitis, but may simulate those 
of a calculus. 

Tuberculosis of the Testicle. — Tliis may be primary or secondary. 
Usually but one organ is involved. The disease is seen in young children 



414 



THE INFECTIOUS DISEASES 



as well as in adults. The process affects chiefly the epididymis, but the 
testis proper may be invaded, and the disease in time extends along the 
vas deferens to the seminal vesicles and prostate. 

Tuberculosis of the Fallopian Tubes and Uterus. — Disease of the 
tubes is much commoner than that of the uterus. The process is usually 
secondary to tuberculous lesions elsewhere and infection may occur 
by direct extension as from the peritoneum or through the blood. ]\Iore- 
over, the possibility of direct infection from the male should be borne 
in mind. 

IX. TUBERCULOSIS OF THE NERVOUS SYSTEM 
Acute tuberculous meningitis is described elsewhere (page 523). 
Aside from this form, tuberculosis occurs in the brain and cord as a 
chronic localized meningitis and in the form of tuberculous tumors 
known as solitary tubercles. These solitary tubercles are met with chiefly 
before the age of fifteen. They may be single or multiple, and consist 
of a firm, rounded, circumscribed caseous mass, sometimes several centi- 
meters in diameter. They are found in the cerebellum, cerebrum, pons 
or spinal cord and do not differ in their symptoms from other varieties 
of tumors. They are usually secondary to tuberculosis in other parts of 
the body. The solitary tubercle is the most frequent type of brain tumor 
in children. (See page 545.) 

LEPROSY 

Leprosy is a chronic infectious disease caused by the bacillus leprae 
and marked by macular skin eruptions and by nodular growths in the 
skin, mucous membranes and nerve tissues. 

Etiology. — The disease has been known for verv^ many centuries. At 
the present time it prevails in China, India, Africa, Norway, in parts of 
Russia, and in the Hawaiian Islands. In this country the disease exists 
in Louisiana, in ]\Iinnesota among the Norwegians, and on the Pacific 
coast among the Chinese. 

The BACILLUS LEPR.^, discovered by Hansen in 1871, closely resembles 
the tubercle bacillus both in morphology and in its staining qualities. 
It is found in great numbers in the specific nodules and in the discharges 
from the nose, throat and the skin ulcers, and in the blood. For many 
years efforts to cultivate the organism artificially failed, but it has re- 
cently been grown together with ameba? and s^Tiibiotic bacteria and 
Duval has obtained pure cultures in media containing tryptophan and 
other free amido-acids. Inoculations of pure cultures have been made in 
animals, and in monkej^s a disease closely resembling human leprosy 
has been produced. 

The disease tends to run in families, but is probably never directly 
inherited. It may occur at any age beyond infancy. Ivong-continued 
and close contact with the disease is usually required for infection, but 
it may occur by means of infected clothing or other fomites. The secre- 
tion from the nose and throat seems to be the chief means of dissemina- 
tion of the contagium. Overcrowding, filth and uncleanly habits arc 



LEPROSY 



415 



strong predisposing influences. Hutchinson believes that infection oc- 
curs through the eating of uncooked fish. 

Morbid Anatomy. — The specific lesion of leprosy is a granuloma 
similar to the tubercle of tuberculosis and the gumma of syphilis. It 
occurs in the form of distinct nodules or tubercles and of diffuse infiltra- 
tions. These growths are composed of small cells and a connective- 
tissue stroma and contain vast numbers of bacilli. They occur chiefly 
in the skin and nerve-trunks, but are also found in the mucous mem- 
branes and in such viscera as the testicles, liver and spleen. These 
growths tend often to break down and form ulcers. 

Symptoms. — The period of incubation is usually two or three years 
in length. Before characteristic symptoms appear there are often for 
weeks or months vague prodromata such as fever, headache, prostration 
and fleeting pains. The first symptom is regularly the appearance in 
the skin of the face, trunk and extremities of hyperesthetic erythematous 
MACULES of varying size, which often become pigmented, but may lose 
their color and grow white and anesthetic. 

Sooner or later the characteristic granulomata develop. When these 
occur chiefly in the skin the type is called tubercular or nodular leprosy, 
when in the nerve-trunks it is known as anesthetic or nerve leprosy. 

Tubercular Leprosy. — Purplish swellings appear in the skin of the 
face, trunk and extremities, which gradually grow into distinct nodules 
or diffuse thickenings. The face is usually the chief seat of these 
growths and is often greatly deformed and thickened leontiasis "). 
Similar growths appear in the mucous membrane of the conjunctivae, 
nose, larynx, etc. Ulceration may cause much destruction of tissue or 
result in deforming scars. Fingers and toes are often destroyed and 
nodules may cause enlargement of the testicle or liver. Ulceration of 
the larynx is common. The patient eventually dies from exhaustion, 
sepsis or some complication. 

Anesthetic Leprosy. — The symptoms after the appearance of the 
macules are chiefly those of a slowly developing neuritis affecting the 
extremities — pain, hyperesthesia, anesthesia, paralysis, contractures, 
trophic disturbances, bullae, gangrene, etc. Along the course of such 
superficial nerve-trunks as the ulnar the nodular swellings can often be 
felt. 

Not infrequently the lesions affect both the skin and nerve-trunks 
and the symptoms of the two types are combined. 

Diagnosis. — In Avell-developed cases the diagnosis is readily made. 
In the early, macular stage, the presence of hyperesthesia or anesthesia 
in the erythematous patches is significant. The bacilli are readily found 
in the discharges of ulcers and in the nodules, or in the blood. 

Prognosis. — ]\Iost cases eventually prove fatal. The average dura- 
tion of life in the tubercular type is eight or ten years. In the anes- 
thetic type it is often twenty or thirty years. 

Treatment. — Some form of segregation is necessary. Attention 
should be given also to the proper disposal of the infectious material and 



416 



THE INFECTIOUS DISEASES 



to the disinfection of fomites. No specific remedy is known, ClianlmngTa 
oil is the drug most esteemed and is given in increasing doses up to 40 
minims three times a day. ]\Iany other remedies have been used, includ- 
ing ichthyol, potassium iodide, bichloride of mercuiy. arsenic, etc. It 
is important that the patient be put under the most favorable hygienic 
conditions and that everything possible be done to improve his general 
health and increase his powers of resistance. 

TETANUS 
(Lock-jaw) 

Definition. — Tetanus is a very fatal infectious disorder, resulting 
from inoculation of a specific bacillus and marked by persistent and 
increasing spasm of the muscles of the jaw, neck and trunk. 

Etiology. — In most cases the disease follows some wound of the body 
surface and especially of the hands or feet. Punctured and badly con- 
tused or lacerated wounds are those most likely to result in tetanus. 
Clean, incised wounds are rarely, if ever, infected. Toy pistol wounds 
seem especially dangerous. Many cases have developed in puerperal 
women, and also in new-born infants (from umbilical infection). Occa- 
sionally no wound is discoverable and the cause has been ascribed to 
exposure to cold. Tetanus occurs endemically in various hot and tem- 
perate countries and is seen at all ages. 

The BACILLUS OF TETANUS is a motile, spore-bearing anaerobic organ- 
ism, found often in the soil, in manure, in street dirt, etc., and it is 
the wounds contaminated by such dirt that are most liable to tetanus 
infection. The anaerobic character of the germ explains why it thrives 
best in deep, punctured wounds. .The bacilli multiply in and about the 
wound, but are found noAvhere else in the body. They produce an extra- 
ordinarily virulent toxin, to whose action upon the motor nerve-centers 
all the symptoms of the disease are due. The toxin seems to reach 
these centers rather by travelling along the axis-cylinders of the periph- 
eral nerves than by means of the circulation. 

Morbid Anatomy. — No constant lesions are found after death. The 
brain and cord often show hyperemia, perivascular exudation, and 
sometimes minute hemorrhages. 

Symptoms. — The incubation period varies from a few days to 
three weeks. In general, the shorter the incubation the more severe 
are the symptoms. These begin with slight stiffness and soreness of the 
muscles of the neck and jaw. The stiffness rapidly increases until 
the jaws cannot be opened (trismus, lock-jaw). Spasm of the other 
facial muscles may produce a curious fixed grin (risus sardonicus") . 
The rigidity extends to the back, chest and abdomen, but the arms and 
legs usually escape. Soon the rigidity is increased by sudden tonic 
spasms of the affected muscles. These last but a fraction of a minute, 
but are usually intensely painful. In them the back may be arched 
so that the body rests only on the head and heels (opisthotonos). These 



FEBRICULA 



417 



tonic spasms become more and more frequent and severe and are induced 
by any slight external irritation, such as a noise or touch. Between 
the spasms there always remains some rigidity. The temperature, as a 
rule, is normal or nearly so until late in the disease, when it gradually 
rises to 103°-105° F. The mind is usuallj^ clear throughout. The 
spasms finally become almost continuous and the patient dies from 
exhaustion or from sudden failure of heart or respiration. 

The DURATION is usually from three to seven days. Mild cases are 
seen which run a more protracted course and end in recovery. A rare 
form — the head-tetanus of Rose — is that which follows wounds of the 
face and is characterized by paralysis of the face on the side of the 
wound, trismus and great difficulty in swallowing. Such cases may 
resemble hydrophobia. 

Diagnosis. — Confusion can hardly occur if the history of the case 
and the progression of the symptoms be carefully considered. The 
bacilli can sometimes be found in the pus of the wounds. 

Trismus alone may appear in hysteria and in such affections as 
quinsy and mumps. In tetany the spasm affects chiefly the extremities. 
In STRYCHNINE POISONING the ousct is abrupt and violent, the rigidity 
is not constant, and trismus is uncommon. 

Prognosis. — Death results in quite three-fourths of the cases. A 
short period of incubation, early fever and the rapid development of 
rigidity are unfavorable signs. 

Treatment. — The wound should be excised or be freely opened, cau- 
terized and treated antiseptically. To lessen the violence of the spas- 
modic paroxysms full doses of chloral or morphine or inhalations of 
chloroform should be used. It may be necessary to feed the patient 
by a catheter passed through the nose. 

An ANTITOXIN has been developed which in animals has been shown 
to neutralize completely the effects of the tetanus toxin, but which 
clinically has proved somewhat disappointing; probably because it can 
rarely be given before the disease is well developed. Some good 
results have been obtained from injecting the antitoxin directly into 
the lateral ventricles of the brain, and very recently a few brilliant 
cures have resulted from its injection into the main nerve-trunks leading 
from the infected region. 

Antitoxin has also been used prophylactically, especially after 
Fourth-of-July wounds, with excellent results. 

FEBRICULA 

(Ephemeral Fever) 

Febricula is not a specific disease, but is merely a term applied to a 
not uncommon type of febrile attack, lasting from one to ten days, in 
which there are no localizing symptoms or signs and in which no cause 
can be ascertained. Such attacks are frequent in children and may be 
27 



418 



THE INFECTIOUS DISEASES 



met with at any age. Many of these eases, especially in children, are 
doubtless of gastro-intestinal origin — indigestion, mild gastro-enteritis, 
food poisoning, constipation, etc., in which fever may be almost the 
only prominent s^nnptom. Other cases are very mild and atypical 
examples of such infectious diseases as typhoid, scarlet fever and 
influenza. Sometimes the cause may be a tonsillitis, pharyngitis, or 
bronchitis, unrecognized because of the slight local signs. Other 
possible causes are otitis media, rheumatic infection, sewer gas poison- 
ing, etc. 

Symptoms.— The fever is usually not high (100°-103° F.), nor 
is the pulse much disturbed. Headache and muscular pains are com- 
mon. The tongue is coated, the appetite lost and the bowels often con- 
stipated. The fever may subside within two or three days or may last 
for a week or more. The patients regularly recover. 

Diagnosis. — The term should be applied to a febrile attack only 
after repeated careful examinations have failed to disclose any of the 
above-mentioned conditions. 

Treatment. — Rest in bed, a fluid diet, a calomel purge and a simple 
diaphoretic mixture are all that is needed in the way of treatment. 

WEIL'S DISEASE 

Definition. — Weil's disease is an acute febrile jaundice, probably of 
infectious nature, which sometimes appears in small epidemics. A bacil- 
lus of the proteus group has been found in the urine and tissues, but 
the true nature of the disease is still uncertain. It is seen chiefly in the 
summer months and in young adult males. Many of the cases have been 
in butchers. 

The only lesions found post-mortem have been fatty degeneration of 
the liver cells, degeneration of the renal epithelium and congestion of 
the viscera and gastro-intestinal mucosa. 

Symptoms. — The disease begins abruptly with a chill, high fever, 
severe muscular pains and headache. Jaundice appears on the first or 
second day, is usually severe and is of the obstructive type, as shown 
by the light-colored stools. The fever lasts from one to two weeks, is 
usually remittent and falls by lysis. There may be delirium or stupor. 
The liver is swollen and tender, and the spleen much enlarged. The 
urine shows evidences of a mild nephritis. Vomiting and epigastric 
pain may be present. Most of the cases recover. 

Diagnosis. — The epidemic character, the high fever and the jaun- 
dice, the swelling of the liver and spleen and the low mortality are 
the chief distinguishing features. Acute yellow atrophy, yellow fever 
and catarrhal jaundice are the conditions most likely to lead to con- 
fusion. 

The TREATMENT is Symptomatic. 



MILIARY FEVER 



419 



MILIARY FEVER 
(Sweating Sickness) 

Miliary fever is an epidemic febrile atfection occasionally seen in 
certain districts in France, Italy and Austria. The epidemics affect large 
numbers of people, but are usually of very short duration. The symp- 
toms are those of fever, profuse sweating and, in the course of three 
or four days, an abundant eruption of miliary vesicles. Most of the 
cases recover within a few days, but the severe form of the disease 
is marked by grave toxemic symptoms and is often fatal. 

GLANDULAR FEVER 

Definition. — This is an acute infectious disease of children marked 
by fever and by inflammation and swelling of the cervical lymph-glands. 
The disease is usually seen in the form of house epidemics. It attacks 
children of all ages, but rarely occurs in adults. Infection is supposed 
to occur through the tonsils or the pharyngeal mucosa, but the exciting 
germ is yet unknown. Some of the cases may be of influenzal nature. 

Symptoms. — The disease begins abruptly with pain and stiffness of 
the neck, fever, headache and often vomiting and abdominal pain. The 
pain and stiffness increase and on the second or third day the enlarge- 
ment of the glands is noticed. This affects chiefly the anterior cervical 
glands, but may involve also the glands in other parts of the body. The 
glands vary in size from a bean to an egg, and are tender and painful. 
Only rarely, however, do they suppurate. The skin is usually not red- 
dened, nor is there much periglandular swelling. There is usually 
enlargement of the spleen and liver. The tonsils and throat show no 
signs of acute inflammation. The acute symptoms subside in ten days 
or two weeks, but the glandular swellings disappear more gradually. 

Suppuration of the glands, otitis media and hemorrhagic nephritis 
are occasional complications. 

Diagnosis. — Other causes of glandular swelling, such as tonsillitis, 
diphtheria and tuberculosis, must be excluded and the epidemic char- 
acter of the disease should be borne in mind. 

The prognosis is good and the treatment palliative and symptomatic. 

MILK SICKNESS 

This is a curious disorder now rarely seen, but at one time prevalent 
and serious in certain of the new settlements west of the Alleghanies. It 
is associated with, and seems to depend upon, an infectious disease of 
the domestic animals (cattle, sheep and horses), called "the trembles." 
The affection is believed to be contracted by eating the meat or drinking 
the milk of diseased animals. 

The symptoms, in man, begin after a few days of vague prodromata 
with severe abdominal pains, nausea and vomiting. There are also fever, 
thirst, obstinate constipation, a tremulous, swollen tongue and a very 
foul breath. In severe cases delirium, convulsions or coma may develop. 



420 



THE INFECTIOUS DISEASES 



The disease may prove fatal within two or three days ; but the symptoms 
usually last from one to three weeks and most of the patients recover. 

ROCKY MOUNTAIN SPOTTED FEVER 
(Tick Fever; Black Fever, or Blue Disease) 

Definition. — An acute infectious disease, closely resembling typhus 
fever, met with in Montana, Idaho and adjacent parts of the Rocky 
Mountains. 

Etiology. — The disease occurs only in mountainous regions and in 
the spring or summer months. It is transmitted by the bite of the 
wood tick, dermacentor occidentalis, and can be conveyed to monkeys, 
rabbits, or guinea pigs by injections of infected blood, but many care- 
ful studies have failed to identify a causative organism. 

Morbid Anatomy. — A petechial rash on the skin, general hypostatic 
congestion, enlargement of the liver and spleen, with degenerative lesions 
in all the viscera are found. Cultures are negative. 

Symptoms. — A fever, rising rapidly, often with chills, continuous 
with moderate remissions, subsiding after two weeks and reaching nor- 
mal toward the end of the third; an eruption, beginning on wrists and 
ankles and spreading to the whole body, at first roseolar, later petechial ; 
severe nervous sjrmptoms, often ending in coma; enlargement of the 
liver and spleen ; digestive disturbances proportionate to the fever, con- 
stitute the essentials of the disease. 

The blood shows a leukocyte count of 8,000 to 14,000. 

Diagnosis. — Typhoid fever can be excluded by the absence of the 
"Widal reaction, the negative blood cultures, and no intestinal lesions, 
but at present no sure criteria distinguish it from typhus fever. 

PELLAGRA 

Definition. — An endemic disease, characterized by an erythema of 
exposed surfaces, marked emaciation, profound melancholia and some- 
times mania. 

Etiology. — Adults from 20 to 50 years, and men especially, are 
attacked. The disease is endemic throughout Southern Europe, par- 
ticularly in Italy, in North Africa, South America, and in some parts 
of the Southern States. Field laborers suffer most frequently. 

It has been attributed to many causes, from exposure to the sun, 
to syphilis, and most persistently to the eating of maize, but none of 
these theories is satisfactory. 

The disease occurs year after year in the early spring months, con- 
tinues through the summer, subsides during the fall and winter. 

Morbid Anatomy. — Emaciation is extreme. The viscera show 
chronic degeneration. The brain and cord show chronic leptomenin- 
gitis with thickening, perivascular infiltration, and degeneration of the 
nerve-cells. 

Symptoms. — A patchy erythema appears on the backs of the hands 
and feet, later on face, arms, legs, and trunk (see Fig. 80). PetecliiaB 



GLANDERS 



421 



or blebs may form on the swollen areas. After a fortnight desquamation 
sets in and the skin becomes dry, rough and brownish. Burning or 
itching accompanies the eruption. 

Weakness, sleeplessness or uncontrollable sleepiness and depression 
are common. 

The tongue is coated, appetite lost, nausea or vomiting often present, 
and constipation the rule. 

Two or three months after the onset the symptoms subside, only to 
recur the next spring. With each recurrence the patient becomes 
weaker, more emaciated and depressed. Periods of maniacal excitement 
with a tendency to suicide develop. Finally the patients become de- 
mented, paralytic, bed-ridden, and die of exhaustion, or from inter- 
current disease. 




Fig. 80. — Pellagrous eruption in stage of desquamation. (International Clinics, Vol. I, Ser. 21.) 



The duration of pellagra varies from two years to ten or fifteen. 

Diagnosis. — The combination with debility and marked nervous 
symptoms is characteristic. 

Prognosis. — If taken early, the disease may be cured. Late cases 
are hopeless. 

Treatment. — Removal from an infected district, good care and tonics, 
especially arsenic, are indicated. 

GLANDER.S 
(Farcy) 

Definition. — A very fatal specific infectious disease of the horse, 
communicable to man, which is marked by granulomatous lesions in the 
nasal and respiratory mucous membranes and beneath the skin. 

Etiology. — The disease is common in horses, asses and mules. In 
man it occurs by inoculation through some break in the skin or mucous 



422 



THE INFECTIOUS DISEASES 



membrane and is seen almost exclusively in stablemen and others who 
work about horses. 

The exciting germ is a small, short, non-motile bacillus, bacillus 
MALLEI, which has peculiar staining qualities and is found abundantly 
in the specific lesions. 

Morbid Anatomy. — The lesions consist of small granulomatous nod- 
ules, composed of lymphoid and epithelioid cells, which tend to suppu- 
rate and break down. They are found in the mucosa of the nose and 
air passages, where they form ulcers; along the course of the subcu- 
taneous lymphatics, where they form abscesses, and in the internal 
organs. When the lesions occur chiefly in the mucous membranes the 




Fig. 8L — The pustular eruption of glanders, often mistaken for small-pox. 

condition is called glanders; when they are chiefly beneath the skin 
it is known as farcy. 

Symptoms. — The incubation period varies from a few days to sev- 
eral weeks and is shortest in the acute and rapidly fatal cases. Both 
glanders and farcy occur in an acute and chronic form. 

Acute glanders runs its course in about a week, and is regularly 
fatal. It begins with fever, pains and prostration. The nasal mucosa 
is much swollen ; the granulomata break down and cause ulceration and 
there is an offensive, purulent discharge. A papulo-pustular eruption 
appears over the face, and often over other portions of the body, which 
may simulate small-pox (see Fig. 81). The patient dies of the intense 
constitutional disturbance or from a complicating pneumonia. 

Chronic glanders shows itself as a chronic nasal and larjoigeal 
catarrh with ulceration. 



PLATE IV. 




Negri bodies (a) in a smear preparation of the hippocampus major of a dog ; stained with eosin 
and methylene blue. (From International Clinics, Vol. Ill, Series 20, page 151.) 



HYDROPHOBIA 



423 



Acute farcy results from infection of the skin and appears as a 
very severe cellulitis with secondary abscesses (''farcy buds") along the 
course of the subcutaneous lymphatics and elsewhere. The disease runs 
the course of a pyemia and is fatal, as a rule, within a week or two. 

In CHRONIC FARCY there are sluggish subcutaneous nodules which 
eventually suppurate and form ulcers. 

Diagnosis. — This depends upon the history of possible infection, the 
clinical picture described and the finding of the bacillus mallei in the 
abscesses. In animals mallein, a glycerine extract of a culture of the 
glanders bacillus, is used subcutaneously as a means of diagnosis. In the 
guinea pig, if pus containing the bacillus mallei be inoculated into the 
peritoneum, within two or three days, a characteristic orchitis is devel- 
oped. This reaction is helpful in the identification of the organism. 

Treatment. — The point of infection should be excised or thoroughly 
cauterized; the abscesses should be opened as they appear, and the 
patient's strength maintained by supportive measures. 

HYDROPHOBIA 
(Rabies) 

Definition. — Hydrophobia is an acute infectious disease of the cen- 
tral nervous system occurring in certain of the lower animals and com- 
municated to man by the saliva of such diseased animals. 

Etiology. — Dogs, wolves and cats are the animals chiefly affected, but 
many other species are susceptible to the disease. Rabies is conveyed to 
man chiefly by the bites of mad dogs, and it is in countries where dogs 
are permitted to roam unmuzzled that most of the cases are seen. In 
Russia many cases occur from the bites of wolves. The disease is 
comparatively rare in this country. 

Probably not more than one-fourth of those bitten by rabid dogs 
develop the disease. Bites upon the face, head and hands (the unpro- 
tected parts) are especially dangerous. The virus is found chiefly in 
the central nervous system and in the saliva. From the point of inocu- 
lation it seems to travel to the cerebrospinal axis along the nerves and 
not by means of the blood or lymph. The nature of the virus is ob- 
scure, but the disease probably depends upon some unknown micro- 
organism. 

Morbid Anatomy. — Lesions are found in the medulla, brain and 
spinal cord. There are degenerative changes in the ganglion cells and 
nerve-fibers, as well as congestion of and exudation from the blood- 
vessels. The mucous membranes of the respiratory and digestive tract 
are much congested. In the cells of the central nervous system, especially 
those of the cornu ammonis and the cerebellum, certain minute bodies, 
the Negri bodies, staining readily by eosin and methylene blue, have been 
found. These Negri bodies (see Plate IV) are minute (1-23/x in diameter) 
round or oval objects whose exact nature is unknown. Negri and others 
regard them as minute protozoa, the causative agents of the disease. 



424 



THE INFECTIOUS DISEASES 



Of this there is no other evidence than their constant presence in the 
nervous system in rabies. The diagnosis of rabies in the dog is now 
confirmed by the examination of the nervous system and the demonstra- 
tion of these bodies. For this purpose a bit of the central nervous sys- 
tem, preferably the cerebellum or the hippocampus major, is crushed 
and a thin smear prepared. This is hardened by immersion in wood 
alcohol for 2 or 3 minutes and then stained. Weak solutions of eosin and 
methylene blue (or Jenner's stain) may be used as for blood. The 
Negri bodies appear as pink or reddish inclusions in the nerve-cells. 

Symptoms. — The period of incubation in man is usually from six 
to eight weeks. It may, however, be as short as two weeks or as long as 
three months. The wound heals promptlj^ and the scar presents no 
unusual appearances. Infection may occur without a wound. 

The symptoms may be divided into three stages: 

(1) A PREMONITORY STAGE, lasting a day or two. during which there 
are restlessness, anxiety, depression and insonmia and often also some 
pain or soreness in the cicatrix. 

(2) The spasmodic stage, in which there are intense excitement and 
restlessness, together with frequent severe and extremely painful spasms 
of the muscles of the larynx and pharjTix. These are excited by any 
attempt at swallowing or by the mere sight or thought of water or by 
any slight external stimulus such as a sound or touch. The spasms 
often involve the muscles of respiration and may amount to a general 
convulsion. The mind is usually clear, but there may be maniacal out- 
breaks. The temperature is somewhat elevated and the pulse grows 
progressively rapid and weak. This stage lasts one or two days and is 
succeeded by — 

(3) A terminal stage of paralysis, which, in man, lasts but a 
few hours, and in which the spasms cease, prostration becomes extreme, 
unconsciousness develops and death ensues. The disease is almost invari- 
ably fatal within four or five days. 

Diagnosis. — Hydrophobia may be closely simulated by a curious 
hysterical condition (lyssophobia) which occasionally develops in those 
who have been bitten by a dog and who are in terror of rabies. There 
may be inability to swallow water, spasms and various other hysterical 
manifestations. Fever is lacking. The SATuptoms subside under suit- 
able moral treatment. 

Treatment. — Prophylaxis. — Rabies can be stamped out by the 
proper muzzling of all dogs and the destruction of such as are ownerless. 

The Avound should be immediately cauterized by strong carbolic acid 
or should be excised. 

It is of the utmost importance to know whether the ofi^ending dog is 
reall}^ suffering from rabies. He should, therefore, be confined, rather 
than shot, since if rabic he will surely die ^vithin a very few days. If 
shot the medulla should be removed and a small portion of it emulsified 
in glycerine or broth and injected beneath the dura mater of a rabbit. 
If rabies is present the animal will die of paralysis (dumb rabies) in 



ANTHRAX 



425 



about two weeks. The demonstration of the Negri bodies as above 
described is now regarded as entirely reliable. 

PRE^^NTIVE Inoculation. — Pasteur's method consists in the daily 
subcutaneous injection of emulsions of the spinal cords of inoculated 
rabbits, the virus having been attenuated by desiccating the cords for a 
certain number of days. This method is almost always successful if 
the incubation period be sufficiently long to allow the proper number 
(12-25) of injections to be made. 

After the disease has developed, treatment is merely palliative and 
consists in attempting to control the spasms by the use of hyoscine hydro- 
bromate (gr. 1/100), morphine or chloroform. 

ANTHRAX 

(Splenic Fever; Malignant Pustule; Wool-Sorters' Disease) 

Definition. — Anthrax is a severe infectious disease of certain do- 
mestic animals, which is due to a specific bacillus and which is occa- 
sionally communicated to man. 

Etiology. — The disease occurs chiefly among cattle, sheep, horses and 
other herbivorous animals, and in certain countries and regions exists as 
a wide-spread and destructive plague. It is not common among the 
animals of this country. 

The specific germ is a very large, non-motile rod — the bacillus an- 
THRACis — which under certain favorable conditions forms extraordi- 
narily resistant spores, and these spores seem to be the chief agents in 
the transmission of the disease. The bacilli are found in the local 
lesions, in the blood and tissues, and in the discharges. In man, anthrax 
is seen almost exclusively among those who are brought in close contact 
with such animals, or with hides, wool, etc., e.g., butchers, drovers, tan- 
ners, wool-sorters, etc. In New York a number of cases have been seen 
among 'longshoremen. Inoculation occurs either through abrasions of 
the skin (external anthrax), or through inhalation or ingestion of the 
virus (internal anthrax). 

Symptoms. — The disease appears in two chief forms: 

(1) External Anthrax or Malignant Pustule. — Inoculation oc- 
curs usually upon the exposed parts, such as the face or hands. At 
the point of infection there appears a small red papule, which rapidly 
increases in size and develops an indurated, inflamed base. At the sum- 
mit of the papule a vesicle forms which soon becomes a blackish, necrotic 
eschar and around this is often formed a circle of secondary vesicles. 
These local appearances are quite characteristic. In the course of two 
or three days the papule develops into a large carbuncle-like swelling 
around which there is much induration and inflammatory edema. The 
neighboring lymph-glands are swollen and tender. During this period 
there is usually a moderate rise of temperature with some constitutional 
disturbance. If the disease is allowed to progress the inflammation 



426 



THE INFECTIOUS DISEASES 



spreads rapidly, the bacilli enter the circulation, the spleen becomes 
much enlarged and the patient usually dies, on the fourth or fifth day, 
with all the symptoms of an intense septicemia. Occasionally no well 
defined pustule forms and there is only a rapidly spreading local edema 
with early septicemia and death. 

(2) Internal Anthrax. — This is less common than the external 
form and results either from infection of the gastro-intestinal tract by 
the ingestion of the flesh of infected animals, or from infection of the 
respiratory tract by inhalation. 

(a) Intestinal Type. {Mycosis Intestinalis.) — There are violent 
gastro-intestinal symptoms, as well as those of septicemia, and the cases 
are usually fatal within a very few days. 

(b) Pulmonary Type. {Wool-Sorters' Disease.) — The symptoms are 
those of a bronchitis or a bronchopneumonia with very severe septicemic 

" constitutional symptoms. 

Diagnosis. — Malignant pustule is usually readily recognized by its 
characteristic appearances and by the finding of the specific bacilli in 
the fluid from the vesicles. The diagnosis of internal anthrax is, how- 
ever, very difficult. The disease may be suspected from the occupation 
of the patient, but a positive diagnosis can hardly be made except by 
finding the bacilli in the circulating blood. 

Prognosis.— The prognosis of internal anthrax is very bad. In 
malignant pustule, if the condition is recognized early and treated 
radically, most of the cases recover. 

Treatment. — The malignant pustule should be promptly and freely 
excised and the wound cauterized thoroughly. The treatment of internal 
anthrax is that of septicemia. 

ACTINOMYCOSIS 

Definition. — A chronic disease of the type of the infectious granulo- 
mata, common in cattle and occasionally seen in man, which is due to the 
streptothrix ACTINOMYCES or ray fungus. 

Etiology. — The disease is frequent in cattle, where it causes a sar- 
coma-like tumor of the jaw, known as "lump- jaw," and is also found 
in horses and swine. Infection seems to occur through the food. The 
ray fungus belongs to a group of organisms closely allied to the bac- 
teria. The germs are found abundantly in the pus from the granulom- 
atous tumors and appear in the form of yellowdsh bodies ("sulphur 
grains") of pin-head size, which consist of masses of radiating threads 
and filaments, many of which show bulbous extremities. In man the 
organism probably finds entrance through carious teeth. 

Morbid Anatomy. — The lesions are not unlike those of tuberculosis. • 
The tumors vary greatly in size and are made up of lymphoid, epithelioid 
and giant cells. In some instances they tend to the formation of much 
connective tissue and in others they break down and form chronic 
abscesses and suppurating sinuses. In half of the cases the lesions occur in 



DISEASES CAUSED BY VEGETABLE PARASITES 427 



the mouth, throat or neck. Less frequently they are found in the 
intestines or lungs and rarely also in the liver, brain, skin and other 
tissues. 

Symptoms. — Most commonly there is a slow growing tumor about 
the lower jaw or in the neck, which eventually suppurates and forms 
fistulous openings. In the lungs the symptoms may be those of fetid 
bronchitis, of bronchopneumonia or of chronic abscess. 

In the intestines there may be tumor or abscess formation. Some- 
times the picture is that of a chronic pyemia. 

The DIAGNOSIS can be made only by finding the characteristic sul- 
phur grains in the pus or in the sputum. The course of the disease 
is very chronic and most of the cases eventually succumb. 

Treatment. — Whenever possible, this should be surgical. In the 
internal forms large doses of potassium iodide should be tried. 

DISEASES CAUSED BY VEGETABLE PARASITES OTHER 
THAN BACTERIA 

Apart from the great variety and number of diseases produced by 
bacteria the investigations of recent years have shown that the human 
organism may be invaded by other vegetable parasites and diseases of 
various types produced thereby. 

Infections of this kind, while of great scientific interest, at present 
are so rare as to be of little practical importance. 

. The lesions produced by these infections are: (1) Cutaneous-gran- 
ULOMATA (nodules or tumors composed of granulative tissue), abscesses 
or ulcerations. 

(2) Internal, subacute or chronic inflammations producing 
nodules resembling tubercles, and, like tubercles, breaking down and 
producing abscesses and chronic suppuration. 

The symptoms, whether of the cutaneous or internal forms of the 
infections, are those of chronic inflammation and suppuration, the lesions 
closely resembling tubercles, and the resulting infection being conse- 
quently commonly mistaken for tuberculosis. 

Among the organisms to be classified under this heading may be 
mentioned : 

(1) Nocardia, organisms midway between bacteria and moulds. They 
resemble bacteria in form, structure and staining properties, while 
they have the fine branching forms and spores or conidia character- 
istic of moulds. They are widely distributed in the air and on grains 
or grasses. 

(2) Actinomyces or ray fungus. (See Actinomycosis.) Granules ap- 
parently indistinguishable from the actinomyces have been found in the 
tropical affection mycetonia, a chronic inflammation of the foot (Madura 
Foot) with abscesses and serous formation closely resembling tubercu- 
losis. The disease is frequent in India and tropical Africa. A very 
few cases have been observed in the United States. 



428 



THE INFECTIOUS DISEASES 



(3) Oidia. Spherical vegetable organisms closely resembling the yeast 
fungus or saccharomyces. These have been found in certain rare skin 
infections, variously denominated blastomycosis or blastomycetic derma- 
titis, psoro-spermiasis, dermatitis coccidiodes, etc. 

(4) Blastomyceies, or yeast fungi, found in certain dermatitis. 

(5) AspergilU or moulds. 

Doubtless, from time to time additions will be made to this list, as 
we now know that man is subject to many other infections than the 
common bacterial types. Practically this possibility is to be borne 
in mind and search made for such parasites in cases resembling external 
or internal tuberculosis, but failing to show the tubercle bacillus. 



IX 



DISEASES CAUSED BY ANIMAL PARASITES 

The importance of pathogenic protozoa in human pathology has been 
recognized only since the discovery of the malarial parasite by Laveran 
in 1880. Tear by year the number of pathogenic protozoa is added to. 
The differentiation of the thousands of varieties of these organisms, a 
few pathogenic, the greater number never found in man, is attended 
with much difficulty. In some cases it is uncertain whether the organism 
belongs to the animal or vegetable kingdom. Any classification at present 
must be tentative. To illustrate the types of protozoa and suggest the 
relationship of kno\\Ti pathogenic types, the following classification, 
abridged from Calkins, is given: 

CLASSIFICATION OF PATHOGENIC PROTOZOA 
Protozoa are unicellular animal organisms which reproduce by 
division or spore formation ; solitary or united in colonies ; free-living 
or parasitic. 

Phylum I. — Sarcodina. — Protozoa with changeable protoplasmic 
processes or pseudopodia. Amebae are included in this class. 

Phylum II. — Mastigophora. — Protozoa with flagella. Trypanosomes, 
circomonas, herpetomonas and the like. 

Phylum III. — Infusoria. — Protozoa with cilia. Balantidium coli is 
the only important example of this class. 

Phylum IV. — Sporozoa. — Protozoa without motile organs and re- 
produced by spores, always parasitic. Plasmodium malariae belongs in 
this class. (See Fig. 82, A, B, C, D.) 

MALARIAL FEVER 
Definition. — Malarial fever or malaria comprises the group of morbid 
conditions produced by the presence in the blood of certain protozoal 
parasites, whose definitive host is the mosquito and whose intermediate 
host is man. 

Etiology. — Malarial fever has been proved beyond doubt to be 
caused by infection with a specific parasite, the Plasmodium malarise, 
transmitted from one individual to another by the bite of a genus of 
mosquito, the anopheles. The spread of malaria in any region therefore 
demands the presence of some individuals having these parasites in 
their blood and of the particular mosquito capable of acting as host 
and transmitting them to man. Where either one of these conditions is 
lacking malaria must die out; where both are present, malaria, unless 
rigid precautions are taken, thrives. The conditions long famed as 
causing malaria are found to be those favoring the fife and activity 
of the malaria-carrying mosquito, the anopheles. The life-history of 

429 



430 



DISEASES CAUSED BY ANIMAL PAEASITES 



the anopheles is the key to nearly all the mysteries which so long sur- 
rounded this subject. 

Mosquitoes of the Genus Anopheles. — The distinctive features of 
these mosquitoes are that both sexes have palpi almost as long as the 
proboscis, that their wings are commonly spotted, the body colors brown 
and yellow, that at rest body, head and beak are carried in one plane, 




Fig. 82. — Types of protozoa. A, Ameba Coli. (After Calkins.) B, Cercomonas Crassicanda. 
(After De Page and Herouad.) C, Balantidium, Entozoon Infusorium. (After Calkins.) D, Spor- 
ozoa, Plasmodium Malarise. (After Ewing.) 



whereas in other varieties there is a marked angle between head and 
body, and finally when resting on any surface the body is not parallel 
but at an angle of about 80° to the surface. 

The eggs are laid in shallow, stagnant water, each female depositing 
from 40 to 100 eggs. In from 3 to 4 days in warm weather the 
larval form develops and lies floating on the surface of the wat.er. In 
from 16 to 20 days the larva develops into a pupal stage lasting from 3 



MALARIAL FEVER 



431 



to 10 days, when the full-grown mosquito emerges. For the development 
of this mosquito stagnant water and a certain degree of warmth (an 
average temperature of at least 60°) are necessary. These mosquitoes 
breed most readily, therefore, in marshes, in the sedgy banks of slow- 
moving streams, in shallow pools or puddles of water, in rain-water 
collected in old cans and the like. The anopheles never fly high or 
far from their birth-place, and the life of any generation is limited 
to about 20 days. They are inactive during the day, except in darkened 
or shady places, while they bite most freely during the night. In these 
facts we find the explanation of the deadly peril of night air in malarial 
districts, of the miasms that rise from swamps, of the freedom from 
malaria enjoyed by mountain resorts, of the prevalence of malaria in 
warm seasons, its subsidence in winter, of the danger of newly-ploughed 
lands (furnishing puddles), of the advantage of cities and towns 
especially under modem hygienic conditions. The reduction in the 
prevalence of malarial fevers brought about by warfare against the 
mosquito, especially on the Panama Canal zone, is most convincing proof 
of their malignant activities. 

Distribution of Malarial Fevers. — In one or another form malaria 
is known from the equator to the Arctic Circle, but the tropics have 
always been the seat of its greatest and most deadly activity. In the 
temperate zone only the milder forms of intermittent or continuous 
fever are seen. In England and in Continental Europe excepting Italy 
malaria is almost unknown. 

Season. — In this latitude malaria is seen during the winter only as 
the recrudescence of an old infection. New cases appear in the spring 
with the development of conditions favoring the development of the 
mosquito, and the disease prevails till the coming of winter. 

Altitude. — The inununity of mountain regions depends on two fac- 
tors, the absence of stagnant water and the lower temperature. If 
conditions are favorable mosquitoes may develop and malaria abound 
in mountain regions. 

Sex and Age. — All ages and both sexes are vulnerable, but malaria 
abounds among children in the tropics, because the mosquito bites them 
by preference. The black races enjoy a certain immunity, acquired, ac- 
cording to Koch's observations, as the result of long-continued infection 
in childhood. 

Recurrence. — In persons suffering from latent malarial infections, a 
chill, fatigue, hunger, or any like influence reducing the vitality may 
precipitate a new outbreak. 

Incubation. — About ten days ordinarily elapse between infection 
with the parasite and the appearance of fever, but this period may be 
protracted by various influences. 

MALARIAL PARASITE OR PLASMODIUM MALARIA 
The organism causing malaria is a microscopic body, of varying 
shape and size, found either in the red blood-cells or the plasma of the 



432 



DISEASES CAUSED BY ANIMAL PARASITES 



patient. It is classed as a protozoan. It cannot, therefore, be grown 
upon culture media like bacteria, nor is it found outside the bodies of 
man or the definitive host, the mosquito. Similar parasites are found 
in the bloods of various mammals, birds, reptiles, fishes. Hundreds of 
varieties have already been catalogued. The Plasmodium malaria shows 
a number of different forms, each associated with a different type of 
fever. 

Tertian Parasite (see Plate V). — In its earlier stage this organism 
is seen as a small, pale ring, with a spot of pigment at some point on the 
margin, lying within a red blood-corpuscle. In fresh blood it shows 
active ameboid movement, constantly changing form and putting out 
pseudopodia. Gradually it increases in size, and niunerous pigment 
granules, dancing actively, appear within it. The blood corpuscles hold- 
ing the parasite become large and pale, sometimes twice the normal size. 

If the blood be deeply stained with Leishmann's or Giemsa's stains 
the hemoglobin of invaded cells is found to be marked by minute specks, 
chromophilic particles, ^'Schuffner's dots." These are distinctive of the 
tertian infection. 

With further enlargement of the parasite the red blood-cell disap- 
pears, is destroyed, and the parasite is set free in the plasma. It then 
appears as a spherical body larger than a red blood-cell, approximating 
in size the white cells, with several pigment granules near the center. 
In this stage two different forms related to the further development 
of the parasite, as intracorporeal or extracorporeal, can be distinguished. 

(a) Certain of these large spherical forms develop evidences of fission 
and finally break up into a number (15-26) of small spherules, each with 
a minute nucleolus, and each of these little spherules undergoes in 
turn the evolution above described, the intracorporeal, endogenous or 
ASEXUAL CYCLE of the malarial parasite. The entire cycle of the tertian 
parasite occupies forty-eight hours. 

(b) Extracorporeal Cycle. — When a number of these spherical 
bodies are taken into the stomach of a mosquito which has drawn the 
blood of a malarial patient, they are quickly differentiated into two 
distinct types, one hyaline, the male element, and the other granular, 
the female element. The male spherules then put out nctivelj^ moving 
flagella (pseudopodia). These flagella finally break away from the 
parent cell and make their way, apparently by their own activity, into 
one of the granular female cells and there disappear. This newly im- 
pregnated spherule then undergoes a series of changes resulting in the 
production of a lance-shaped or vermicular body possessed of distinct 
powers of penetration. This body makes its way into the muscular wall 
of the stomach of the mosquito, and there undergoes development into 
a cyst-like form, which subdivides into a number of spindle-shaped bodies 
contained within a capsule. In the end the capsule ruptures and the 
spindle bodies are discharged into the body cavity of the mosquito. 
Thence they make their way, probably by the blood stream, to the salivary 
glands of the insect. From the salivary glands the proboscis opens by 



PLATE V. 



The Parasite of Tertian Fever. (Drawn by Mr. Brodel for Thayer and Hewetson's paper. 
The Malarial Fevers of Baltimore, Johns Hopkins Hospital Reports, Volume V. We copy 
the original legend.) 

I. Normal red corpuscle. 
2, 3, 4. Young hyaline forms. In 4, a corpuscle contains three distinct parasites. 
5, 21. Beginning of pigmentation. The parasite was observed to form a true ring by the con- 
fluence of two pseudopodia. During observation the body burst from the corpuscle, 
which became decolorized and disappeared from view. The parasite became, almost 
immediately, deformed and motionless, as shown in Fig. 21. 
6, 7, 8. Partly developed pigmented forms. 

9. Full grown body. 
10-14. Segmenting bodiesi. 

15- Form simulating a segmenting body. The significance of these forms, several of which 
have been observed, is not clear to the writers, who have never met with similar 
bodies in stained specimens so as to be able to study the structure of the individual 
segments. 
r6, 17. Precocious segmentation. 
18, 19, 20. Large swollen and fragmenting extra-cellular bodies. 
22. Flagellate body. 
23, 24. Vacuolization. 

The Parasite of Quartan Fever. 

25. Normal red corpuscle. 

26. Young hyaline form. 

27-34. Gradual development oi the intra-corpuscular bodies. 

35. Full grown body. The substance of the red corpuscle is no more visible in the fresh 
specimen. 
36-39. Segmenting bodies. 

40. Large swollen extra-cellular forms. 

41. Flagellate body. 

42. Vacuolization. 



PLATE V. 

The Parasite of Tertian Fever 



• m 0 








MALARIAL FEVER 



433 



a long duct and through this channel these spindle bodies are discharged 
into the blood of a person bitten by the infected mosquito. In the blood 
of the new host the spindle bodies enter the corpuscles and there develop 
into the intracellular forms already described. 

The extracorporeal cycle of the malarial parasite occupies about 
two weeks' time. 

Quartan Parasite. — This organism in its earliest forms is a small 
round body in a red cell, smaller than the tertian variety. Its ameboid 
movement is much less active, and as soon as it becomes pigmented, 
ceases entirely. The pigment granules are coarse and the total amount 
is large. Segmentation occurs in a manner suggestive of the petals of 
the daisy around a relatively large mass of centrally placed pigment. It 
finally divides into eight to ten segments, as compared with the 16-26 
of the tertian parasite. The quartan organism does not cause marked 
enlargement of the cells in which it lies — but when mature completely 
fills them. The "daisy" segmenting form is more frequently seen in 
the peripheral blood than the corresponding phase of other parasites. 
By these characters the quartan parasite can ordinarily be readily 
distinguished. Its complete intracorporeal cycle occupies 72 hours. 

Estivo- Autumnal Parasite (see Plate VI). — Parasite of malignant 
malarial fevers. The earliest form of these is a minute unpigmented 
ring, discoverable only with difficulty, in the red cells. Multiple infec- 
tion of individual corpuscles is more common than with other forms. It 
is also characteristic that the parasites are relatively infrequent in the 
peripheral circulation, but are found in great numbers in the capillaries 
and small arteries of the deep viscera (especially the spleen) and the 
bone marrow. They are, therefore, sometimes discovered only after 
death. These parasites tend to produce a peculiar shrinking of the in- 
fected corpuscles, so that many of these become crenated and very 
dark, the so-called "brassy bodies." The larger pigmented forms of 
this parasite, corresponding to the fully developed tertian or quartan 
varieties, are rarely seen in the peripheral blood. Instead, there appear 
either in the red cells or free in the plasma certain crescentic forms or 
crescents, which are characteristic of the organism. These crescents 
are longer than the red cells, slightly curved, the ends rounded, with 
definite pigment masses near the center of the body. They may appear 
as though attached to a red cell, a part only of the body of the latter 
showing in the bay of the crescent, or may be free in the plasma. Con- 
trary to the behavior of the other forms of the malarial parasite, they 
do not at once disappear from the peripheral blood on the administra- 
tion of quinine, but may persist for from three to six weeks. The life 
span of the estivo-autumnal organism, owin^- to the difficulty of finding 
mature forms, is much less accurately kno\\Ti than those of the tertian 
or quartan forms, but is calculated at from 24 to 48 hours. 

Both the quartan and estivo-autumnal forms undergo an extracor- 
poreal cycle analogous to that of the tertian parasite. 

Morbid Anatomy. — The milder malarial fevers seen in this latitude 
28 



434 



DISEASES CAUSED BY ANIMAL PARASITES 



— quotidian, tertian or quartan — are rarely fatal and their anatomical 
changes must be inferred from those of pernicious malarial fever or 
cachexia. In these conditions the skin and mucous membranes are very- 
pale, and the skin has an icteric tint, but the scler^e are clear. The 
blood, besides the presence of the parasites, shows a marked secondary 
anemia, by reduction both of cells and hemoglobin, particularly the 
latter. The leukocytes are usually moderately increased — 10,000 to 
15,000 — with an increase in the percentage of large mononuclears. The 
leukocytes frequently show pigmentation with hemozoin derived from 
the parasites. The plasmodia are often found most abundantly in the 
blood of the spleen, liver, or bone marrow. 

The spleen is greatly enlarged and very soft, diffluent. It is often 
deeply pigmented. 

The liver is large, soft, congested and also pigmented. Two forms 
of pigment are found in both these organs — (a) hemozoin derived from 
the parasites; (b) hemosiderin from the hemoglobin of destroyed red 
cells. Other organs, the lungs, kidneys, intestines, may show like pig- 
mentation. 

Acute nephritis, myocardial degeneration with dilatation of the heart, 
pneumonia, or empyema and dysenteric lesions of the colon may be 
found. 

Symptoms. — Incubation. — In experimental infections, the latent 
period has been from 2 to 10 days. Susceptible persons may, however, 
dwell in malarial regions for some time before seizure. The United 
States soldiers, serving in Cuba, as a rule, had been there a month 
or more before developing symptoms. 

For clinical purposes we distinguish four groups of eases: 1. Regu- 
lar intermittent fevers — quotidian, tertian, quartan. 2. Irregular re- 
mittent or continued fevers — estivo-autumnal fever. 3. Pernicious 
forms. 4. Malarial cachexia. 

I. THE REGULAR INTERMITTENT FEVERS 

The characteristic feature of these fevers is the recurrence at definite 
intervals of the malarial paroxysm, marked by chill, fever and sweat- 
ing. A period of several days or a week of indefinite malaise, with loss 
of appetite, a coated tongue, and slight headache, precedes the develop- 
ment of typical chills. Once the chills begin they are repeated with 
almost clock-like regularity at definite intervals, every day (quotidian) 
or every second (tertian) or third day (quartan). The chills occur 
most often in the early afternoon, sometimes in the morning, extremely 
rarely at night. (See Pig. 83.) 

In the typical paroxysm three stages are distinguished. 

TiTE CHILL sets in suddenly with a feeling of coldness in the back and 
extremities. The skin becomes pale and cold, the lips may be blue, the 
pulse small, feeble and either slow, normal, or quickened in rate, and 
the patient is greatly prostrated. Soon the teeth begin to chatter and 



PLATE VI. 



The Parasite of ^stivo-Autumnal Fever. (Drawn by Mr. Brodel for Thayer and Hewetson's 
paper, The Malarial Fevers of Baltimore, Johns Hopkins Hospital Reports, Vol. V. We copy 
the original legend.) 
1,2. Small refractive ring-like bodies. 
3-6. Larger disc-like and amoeboid forms. 

7. Ring-like body with a few pigment granules in a brassy, shrunken corpuscle. 
8, 9, 10, 12. Similar pigmented bodies. 

II. Amoeboid body with pigment. 

13. Body with a central clump of pigment in a corpuscle, showing a retraction of the 
haemoglobin-containing substance about the parasite. 
14-20. Larger bodies with central pigment clumps or blocks. 

21-24. Segmenting bodies from the spleen. Figs. 24-27 represent one body where the entire 
process of segmentation was observed. The segments, eighteen in number, were 
accurately counted before separation as in Fig. 28. The sudden separation of the 
segments, occurring as though some retaining membrane were ruptured, was observed. 

29-37- Crescents and ovoid bodies. Figs. 34 and 35 represent one body which was seen to 
extrude slowly and, later, to withdraw two rounded protrusions. 

38, 3(9. Round bodies. 

40. " Gemmation," fragmentation. 

41. Vacuolization of a crescent. 

43-44- Flagellation. The figures represent one organism The blood was taken from the 
ear at 4.15 p.m.; at 4.17 the body was as represented in Fig. 43. At 4.27 the flagella 
appeared; at 4.33 two of the flagella had already broken away from the mother body. 

45-49. Phagocytosis. Traced by Dr. Oppenheimer with the camera iucida. 



The Parasrte of Aestivo Autumnal Fever. 




MALARIAL FEVER 



435 



the limbs to shake (rhythmic contractions) ; the pallor, blueness and weak- 
ness of the pulse are increased. The surface temperature during this 
time is low; the internal (rectal) temperature, normal at first, is raised 
several degrees. Headache may be severe, and nausea and vomiting are 
frequent. After from one-half to two hours the hot stage succeeds. 
From the chilly condition the patient quickly passes to one of burning 
fever; the face flushes, the conjunctivae become suffused, the skin hot 
and dry, the pulse rapid, full and bounding. The headache is intense, 
the patient excited, delirious, stupid or comatose. Nausea and vomiting 
may occur during this period. The temperature reaches 104° -106° F., 
or even more. A general erythema or urticaria may appear. This stage 
lasts from two to six hours and is followed by sweating. Perspiration 
begins on the face and neck and soon breaks out over the whole body 
and the fever begins to fall. The sweating becomes profuse and drench- 
ing. The temperature falls to normal or below, all the signs of dis- 




Fig. 83. — Temperature of tertian malaria, three paroxysms. 



turbance vanish, and the patient, though weak, feels quite comfortable 
till the recurrence of the paroxysm. (See Fig. 84.) 

More or less definite anemia and enlargement of the spleen regularly 
develop in patients undergoing these paroxysms. In the first days 
neither may be notable, but with each recurrence they become more 
marked and in advanced cases both are extreme. The splenic enlarge- 
ment of malarial fever is important, the spleen usually being larger than 
in any other febrile condition, second in size only to the tumors seen 
in leukemia or Ilodgkin s disease. Herpes labialis is often present. 

Relation of Paroxysms to Plasmodia. — Each chill is found to be 
coincident with the maturation of a group of parasites in the patient's 
blood. The tertian parasite's life-cycle is 48 hours, with a single infec- 
tion the patient has chills every second day (tertian fever). Similarly 
the life-cycle of the cpiartan parasite being 72 hours, the chills would 
recur every third day (quartan fever). Double infections with the 



436 



DISEASES CAUSED BY ANIMAL PARASITES 



tertian parasite, one group maturing every twenty-four hours, give 
rise to daily chills (quotidian fever). The same result may theoretically 
be brought about by infection with three distinct groups of the quar- 
tan parasite. Double infections with the quartan organism give chills 
on two successive days with a single day's interval. 

Course. — Once established such paroxysms may go on indefinitely 
unless treated effectively. On the other hand, they may spontaneously 
cease at any time and the patient enjoy an indefinite period of freedom 
till the lowering of his vitality from any cause (exposure to cold and 
wet, fatigue, fright, etc.) causes a new outbreak. 

Recurrences are very common. These intermittent fevers are rarely 
fatal, but in the tropics any form of malaria may develop the characters 
of the pernicious fever. 

Diagnosis. — The periodicity. Malarial chills tend to return at the 
same hour of the day. The enlarged spleen, the rapidly developed 




Fig. 84. — Quotidian malaria, daily paroxysms. 



anemia make the intermittent fevers easilj^ recognizable. The diagnosis 
is made certain by the presence of the parasites. These are best sought 
for about the time of the chill, when they are most mature, but may 
be found at any time. ]\Iore than one examination may be required. 
Quinine should not be given before the examination, for the drug quickly 
causes the disappearance of the parasites from the peripheral circula- 
tion even when it does not check nor stop the paroxysms of fever. 

The chills of sepsis such as occur in pyemia or advanced tubercu- 
losis may simulate malaria, but they are never so regular. In pyemia the 
chills, moreover, recur at irregular intervals day or night. The parasites 
of malaria are not to be found in the blood. Neither the anemia nor the 
splenic enlargement, though present, is as pronounced as in malaria; 
a leukocytosis and increased polynuclear percentage may be sho\m by 
the blood, or blood cultures may yield bacteria. There will develop 
localized symptoms of suppuration in some part or parts. 



MALARIAL FEVER 



437 



In advanced tuberculosis chills and sweating may recur each after- 
noon, but there are local (pulmonary, osteal or glandular) signs of the 
disease, bacilli in the sputum, and no parasites in the blood. 

Finally none of these fevers yields to quinine ; the malarial inter- 
mittent fevers are promptly cured by it. 

II. IRREGULAR REMITTENT OR ESTIVO-AUTUMNAL FEVER 
It is extremely difficult to describe the various types of fever which 
may be caused by infection with the estivo-autumnal parasite. Tem- 
perature curves of endless variety may be shown. The fever may be very 
slight or very high, continued, or remittent, or may come and go in such 
manner as to make it impossible to classify the curve. 

Whatever the type of fever, chilly sensations, or distinct chills may 
accompany the rises and sweating occur with the falls. The patient 
regularl}^ becomes markedly anemic and the spleen is notably enlarged. 
Irregular fever, anemia and a large spleen may be termed the funda- 
mental features. 

The estivo-autumnal infections are likely to be persistent and severe. 
In the temperate regions they constitute the only severe malarial cases. 
In the tropics, although any malarial fever may become severe and 
dangerous, the estivo-autumnal or ''crescent " infections constitute the 
great bulk of cases of so-called pernicious malarial fever. 

Among the more common types of estivo-autumnal fever the follow- 
ing may be cited : 

(1) The Continued Fever Resembling Typhoid. — The patients give 
a history of malaise and fever with gastric and intestinal disturbance 
lasting for one or tw^o weeks. They have a continued fever, possibly more 
irregular than the usual typhoid chart, but not easily distinguished 
from it; they suffer from headache, prostration, diarrhea or constipa- 
tion, pains in the back and limbs; the appearance is that of typhoid 
fever, and the disease is frequently mistaken for it. The spleen, however, 
is larger than is ordinarily met with in typhoid, the anemia is more 
marked, there are no rose spots, no Widal reaction, no bacilli in the 
blood, but on examination (repeated, if necessary) the parasites, es- 
pecially the crescentic forms, are found. 

(2) A Remittent Type. — This differs from the latter only in the fact 
that the morning recessions of the fever are more marked. From the 
fact that this type of fever is specially often accompanied by severe 
vomiting and purging and possibly jaundice, the term bilious remittent is 
often used. 

(3) Irregular Intermittent Types. — Various intermittent fevers, re- 
sembling but not conforming to the type of ordinary quotidian, tertian 
or quartan fever, may be produced by crescent infections. 

In these irregular types chills, fever and sweating may occur, but 
these symptoms are much less marked and less characteristic than in 
the simple tertian or quartan infections. The disease is severer and 
is more likely to attain the so-called pernicious, i.e., a very severe, form. 



438 DISEASES CAUSED BY ANIMAL PARASITES 



The notable symptoms in these pernicious types, in addition to the fever, 
anemia and splenic tumor, are : — 

(1) Cerebral. — Headache, delirium, hemiplegia or coma may de- 
velop. In some cases these intense cerebral disturbances come at the out- 
set, more often during the course of the disease. They are explained 
by blocking of the brain capillaries by large numbers of the parasites. 

(2) Gastro-intestinal. — Nausea, persistent vomiting, often becoming 
bile-stained (bilious), and diarrhea, even dysenteric in type, may occur. 
Jaundice may accompany the severe gastric symptoms. Severe malarial 
fever accompanied by persistent vomiting and jaundice, therefore, often 
suggests yellow fever. Similarly many of the patients returning from 
the Philippines had dysenteric sjTnptoms. 

(3) Constitutional Collapse. — At any time during severe malaria 
s^Tnptoms of collapse may develop. In this condition the patient is 
profoundly exhausted, the pulse rapid, feeble and intermittent, the 
surface pale, cold and bathed in perspiration, the eyes sunken, the lips 
and finger tips cyanotic — the algid or, if vomiting and purging be pres- 
ent, the choleraic type of the disease. 

III. MALARIAL CACHEXIA 

As the result of repeated attacks of malarial fever, especially of the 
estivo-autumnal type, a condition of extreme anemia and profound 
exhaustion, with enormous enlargement of the spleen (ague cake) , may be 
produced. The patients present the pallor, palpitation, dyspnea, con- 
stipation, or diarrhea, possibly edema of the ankles, characteristic of 
profound anemia. The spleen projects below the edge of the ribs and 
may occupy the whole left side of the abdomen. The urine may show 
albumin and casts. 

The explanation of the irregularity of the symptoms in estivo- 
autumnal fever appears to be that there are a number of different 
groups of organisms, each maturing at a different time. The toxins 
produced by these organisms seem also to be of a peculiarly virulent type. 

Sequelae. — Profound mental disturbances, explained by the blocking 
of the capillaries of certain cortical regions by parasites, may occur. 
Melancholia, mania, or delusional insanity may be met with. Chronic 
nephritis, severe anemia and chronic enlargement of the spleen are also 
possible results of severe or repeated attacks of fever. 

Diagnosis. — In New York the diagnosis of malarial fever is ex- 
tremely easy. The great majority of cases are typical tertian or quotidian 
fever; quartan fevers are very rare. The estivo-autumnal infections are 
of the typhoid type and without laboratory aids may easily be mistaken. 
But if the Widal reaction is tested and blood cultures are employed, the 
blood examined for plasmodia, and the effects of quinine tried, there is 
little chance of error. 

Mild irregular fevers due to malaria may easily be overlooked if 
blood examinations are not made. 

In the tropics, on the other hand, malaria is protean in type and 



MALARIAL FEVER 



439 



easily confused with typhoid or yellow fever, cholera, dysentery, sepsis 
or tuberculosis. It is, therefore, clear that mistakes can be avoided only 
by having the facts constantly in mind and employing the laboratory 
methods which are essential to diagnosis. Long tables of differential 
diagnosis are much less important than the examination of the blood for 
parasites, or for typhoid bacilli, or the stools for ameba or the cholera 
vibrio, etc. The administration of quinine should not be begun till the 
blood has been examined for the parasites. 

The suggestive features of all malarial fevers are the fever, anemia, 
and enlarged spleen. 

Prognosis. — The malarial fever of these latitudes is benign. It 
yields promptly to quinine in moderate doses. In neglected cases the 
anemia and prostration may become profound. 

In the South and in the tropics malaria is a severe and often deadly 
disease, yet the report of Colonel Gorgas for the year 1909 shows that 
of 10,000 malarial patients on the Isthmus of Panama but 52 died 
during that year — as remarkable a tribute to the advantages of early diag- 
nosis and adequate treatment as is the limitation of the disease to the 
sanitary methods employed. 

Prophylaxis. — The prevention of malaria follows three general lines : 
(1) the destruction of the breeding places of the insects and the insects 
themselves. 

The measures required in the destruction of the breeding places are 
the drainage of marshes, pools, puddles, etc., or the covering with petro- 
leum of such stagnant waters as cannot be drained, the clearing away 
of brush and under-growth about habitations, the removal or screening 
of all waters in cisterns and the like. 

(2) The prevention of infection of the mosquitoes by preventing their 
approach to malarial patients by screening hospitals or keeping netting 
over the beds. (3) Protection of individuals in malarial neighborhoods 
by screening the houses, and by the periodic administration of quinine, 
two" or three grains thrice daily. 

Treatment. — For many mild cases of intermittent fever, an initial 
dose of calomel and 5 grains of quinine sulphate in capsule three times 
a day is all that is required. For severer cases rest in bed and a light 
or fluid diet may also be ordered. Some prefer to give the quinine in 
one large dose, 15-20 grains, 3 or 4 hours before the time for a chill. 
Small doses of quinine should be given for many weeks after the cessa- 
tion of the chills and repeated each spring and summer to avoid return. 

In the estivo-autumnal fevers, especially in the pernicious forms, an 
initial purge is followed by one large dose of quinine, and then 5 grains 
every 3 or 4 hours. As much as 40 grains a day may be required for 
several weeks before the fever is conquered. If vomiting occurs or 
the patient cannot swallow, the quinine may be given hypodermatically, 
the bihydrochloride or bihydrobromide being used because of their ready 
solubility. After recovery the patient should from time to time take 
quinine in small doses, 2 grains thrice daily, for a week at a time to 



440 



DISEASES CAUSED BY ANIMAL PARASITES 



prevent relapses. Anemia must be treated by iron and arsenic. Malarial 
cachexia calls for removal to a healthful climate, baths and saline mineral 
waters such as are had at various watering places, and the proper treat- 
ment of the anemia. 

BLACK-WATER FEVER— HEMOGLOBINURIC FEVER 

Definition. — A fever of tropical and subtropical countries whose 
chief symptom is the passing of hemoglobin in the urine. 

Etiology. — Two radically divergent views are held. (1) That black- 
water fever is merely a pernicious malarial fever, the outbreaks of 
which, for reasons unknown, are closely associated with the taking of 
quinine. (2) That the fever is not malarial but is caused by infection 
with some as yet unknown organism. 

The fever is met with in all tropical and sub-tropical regions, its 
distribution being that of severe malarial fevers. It has occasionally 
been observed in the Southern States. Tropical Africa and India are 
the favorite seats of the disease. It is never found except in people 
who have had malaria, especially in those who have had repeated attacks. 
In the tropics it frequently occurs in epidemic form. 

Morbid Anatomy. — The liver and spleen are enlarged, soft and 
show degeneration with the presence of hemozoin and hemosiderin. The 
kidneys are enlarged, congested, the tubules perhaps blocked by hemo- 
globin infarcts, and pigment present in the capillaries and cells. 

Symptoms. — The period of incubation is entirely unknown. The 
onset is sudden with chill, fever and sweating, as in malaria. With the 
paroxysm there is aching in the loins or over the bladder and the urine 
passed is found to be very dark, a deep red or black. Jaundice quickly 
develops. Persistent vomiting of bile-stained fluid is common. 

The course of the disease is extremely irregular. A single paroxysm 
may be all, or the fever may continue like an atypical malaria for days 
or weeks, the hemoglobinuria, jaundice and vomiting following the rise 
and fall of the fever. During the attacks both spleen and liver are 
enlarged. 

The urine in black-water fever is deep red or black, with a heavy 
brownish-gray sediment. Albumin is present in large amount, and 
hyaline and granular casts and much granular material are found. Red 
blood-cells are few or absent. Spectroscopic examination of the urine 
shows the double band of oxyhemoglobin or the bands of methemoglobin. 

Diagnosis. — The disease must be distinguished from paroxysmal 
hemoglobinuria, yellow fever, malarial fevers and icterus gravis. Parox- 
ysmal hemoglobinuria bears no relation to previous malarial attacks and 
is a milder affection. So far as the initial attack is concerned the phe- 
nomena of hemoglobinuric fever and paroxysmal hemoglobinuria are the 
same. 

The only distinguishing point from certain irregular types of malarial 
fever is the absence of the plasmodia. Some authors insist that the 



SYPHILIS 



441 



parasites can be found by sufficiently careful examination and that the 
disease is malarial. 

From yellow fever the disease is distinguished by the severity of 
onset, the early jaundice, and the hemoglobinuria. Hematuria occurs in 
yellow fever, but blood pigment is not found without the red cells. 

Prognosis. — The mortality is high, 25 per cent. Many attacks are, 
however, mild, and may be often repeated without fatality. The severity 
of the disease varies in localities and in different epidemics. 

Treatment. — This must vary with the conception of the disease. 
Some treat it as severe malaria by an initial dose of calomel followed by 
heroic doses of quinine, as much as 120 grains per day. Others say that 
quinine causes the hemoglobinuria and withhold it. 

Rest in bed, the administration of fluids, especially water, according 
to the condition of the stomach, enemata of physiological salt solution or 
hypodermoclysis and cups or hot fomentations to the loins constitute the 
rational treatment of the disease. A combination of 10 grains of sodium 
bicarbonate and bichloride of mercury gr. 1/30, given every two hours, 
is said to be of value. 

SYPHILIS 
(Lues) 

Definition. — Syphilis is a specific infectious disease of very chronic na- 
ture which is communicated either by direct inoculation or by hereditary 
transmission. The acquired form is marked (1) by a local initial lesion; 
followed after a few weeks (2) by constitutional symptoms and eruptions 
upon the skin and mucous membranes (secondary lesions), and, after 
a much longer interval, usually by (3) specific growths in the various 
viscera and tissues (tertiary lesions). In the hereditary form the initial 
lesion is lacking. 

Etiology. — Syphilis has been known for many centuries. It is world- 
wide in distribution, attacks all races and may be acquired at any age. 
In this country it is especially prevalent among the negroes. The specific 
organism of syphilis is, in all probability, the protozoan parasite first 
observed by Shaudinn and Hoffman in 1905. The organism, a delicate 
spirochete (spirocheta pallida), is found generally in the local lesions 
and in the blood of the patient. While the organism is regularly found 
in syphilis, and not in other conditions, in man, and also in animals 
(monkey, rabbit) inoculated with syphilis, it has not yet been isolated 
by cultural methods and, therefore, the final proof of its causative rela- 
tion to the disease is still lacking. 

Modes of Infection. — The disease is communicable usually during 
its primary and secondary stages. The virus resides in the secretions of 
the open sores, in the blood, saliva, etc., and gains entrance usually 
through abrasions in the skin or through a mucous membrane. 

Inoculation. — This occurs in most cases upon the genitalia during 
sexual intercourse. It may occur, however, upon the lips, tongue, tonsils^ 



442 DISEASES CAUSED BY ANIMAL PARASITES 



nipples, fingers, etc., by direct contact, as in kissing, suckling, vaginal 
examination, etc., or by means of infected implements such as razors, 
dental instruments, pipes and eating utensils. Inoculation has occurred 
rarely in the operations of vaccination, tattooing and circumcision. 

Hereditary Transmission. — The chances of transmission are greatest 
when both parents are diseased. A syphilitic man or woman may, how- 
ever, transmit the disease to the offspring without the other parent 
being infected. A healthy woman who has borne a syphilitic child is 
herself immune from infection from the child, although she presents no 
evidence whatever of the disease (Colics' Law). If a woman become 
infected after conception the child may or not develop the disease (pla- 
cental transmission). 

One attack of syphilis usually provides immunity for life. Only 
rarely have instances of a second infection been recorded. 

Morbid Anatomy. — The initial lesion (primary sore or chancre) forms 
at the point of inoculation. There are infiltration of the skin ^\dth round 
cells, proliferation of connective-tissue cells and often the formation of 
giant cells. The neighboring small arteries are the seat of an obliterating 
endarteritis. The adjacent lymph-glands show hyperplasia and indura- 
tion. The SECONDARY LESIONS include various skin eruptions, mucous 
patches, warts and condylomata, iritis, etc. 

Tertiary Lesions. — The most characteristic of these is a circum- 
scribed granulomatous growth, called gumma or syphiloma, varying in 
size from a millet seed to an egg, and found in the skin, mucous mem- 
branes, bones, muscles, and the various viscera. These growths, which 
resemble closely the specific growths of leprosy and tuberculosis, usually 
undergo caseation at the center and sclerosis at the periphery, but in 
the skin and mucous membranes they frequently soften and ulcerate. 
Diffuse fibrosis of the viscera, amyloid degeneration and arteritis also 
occur as late lesions. 

ACQUIRED SYPHILIS 
Symptoms. — The incubation period is usually from three to five 
weeks. 

Primary Stage. — The initial lesion or chancre appears as a small 
red or purplish papule which slowly enlarges, becomes dense and in- 
durated at its base and margins, and usually undergoes superficial ulcera- 
tion. It is almost always single. The adjacent lymph-glands also show 
induration and enlargement. 

Secondary Stage. — This is marked chiefly by constitutional symp- 
toms and by eruptions upon the skin and mucous membranes. The symp- 
toms develop between six and twelve weeks after the appearance of the 
chancre. There are fever, usually slight and transient, but sometimes 
severe and of a continued, remittent or intermittent type; headache, 
usually worse at night ; prostration ; anemia ; and nocturnal pains in 
the bones and joints. 

Skin Eruptions {Cutaneous Syphilides) . — These are of various 



SYPHILIS 



443 



types, all of which tend to be symmetrical in distribution and free from 
itching and pain. The earliest form is the syphilitic roseola — macular 
spots of pink or reddish color seen chiefly on the abdomen and chest. 
Later rashes may be papular, pustular, squamous, etc. Of these the 
papular syphilide is the commonest. It has a coppery^ or ''raw-ham" 
color, is apt to invade the forehead (corona veneris), scalp, face, the 
region of the genitals and the palms of the hands and soles of the feet, 
and usually lasts for many weeks. The pustular eruption may closely 
resemble that of small-pox ; the squamous, that of psoriasis. In the moist 
skin about the anus, perineum and genitals the papules form large, flat 
growths with excoriated surfaces (flat condylomata). 

The Mucous Membranes. — Sore throat is common. It may be due to 
simple hyperemia, to ulcers upon the tonsils or pharynx, or to mucous 
patches. These are slightly excavated areas, covered b}^ a grayish 
pellicle, and seen on the tonsils, fauces, tongue, inner surface of the 
cheeks, and about the vulvar and anal orifices. Hypertrophy of the 
papilla may produce the so-called syphilitic wart or papillomata. The 
larynx may be inflamed and ulcerated. 

Other Symptoms. — General, slight enlargement of the lymph-nodes 
is usual, as is also alopecia. Iritis, retinitis, periostitis, and onychia are 
occasional symptoms. 

The symptoms of the secondary stage usually last from six months 
to a year, although with energetic treatment they may sometimes subside 
within a few weeks. They vary much in number and severity. Certain 
cases are marked by a very unusually severe and intractable course (ma- 
lignant syphilis). The disease is infectious throughout this period. 

Tertiary Stage. — Tertiary symptoms are altogether wanting in the 
great majority of the patients. In untreated cases they develop in from 
20 to 25 per cent. In those thoroughly treated the percentage is reduced 
to five or less. An interval of two or three years usually elapses between 
the secondary and the tertiary manifestations, but the latter may not 
appear for ten or even twenty years. 

The skin eruptions are scanty, asymmetrical and tend to involve the 
deeper layers of the skin and to ulcerate. They may be tubercular, ser- 
piginous, bulbous or rupial in type. 

In the eye iritis, retinitis or chorioiditis may occur. 

Nodular thickenings of the periosteum of the long bones, sternum and 
skull are common. 

Gum M ATA occur in the subcutaneous and submucous tissue, and in 
the muscles^ bones and internal organs. In and beneath the skin and 
mucous membranes they are prone to soften and ulcerate. In the 
deeper tissues they usually undergo sclerosis (see Fig. 85). 

Syphilis of the Digestive System. — Gummata occur not infrequently 
in the soft palate and pharynx. Syphilis of the esophagus, stomach and 
intestines is very rare. In the rectum gummata sometimes occur (almost 
always in women) and eventually lead to cicatricial stricture. The liver 
is often attacked both in acquired and in inherited syphilis. The lesions 



444 



DISEASES CAUSED BY ANIMAL PARASITES 



are of three types (a) a chronic perihepatitis, (b) diffuse interstitial 
hepatitis (syphilitic cirrhosis) and (c) ^mmata. These latter vary much 
in number and size and are usually associated with nodular enlargement 
of the organ. These caseous masses sometimes undergo softening and 
suppuration but usually they become sclerotic and often leave deep and 
deforming scars. The symptoms of liver syphilis are usually those of 
cirrhosis, although the gummatous nodules may closely simulate a ma- 
lignant growth. Often there are no symptoms whatever. 

In addition to the above lesions syphilis not infrequently results in 
AMYLOID DEGENERxiTiON of the livcr, splccu, kiducys, etc. 

The Vascular System. — The heart muscle may be the seat of gum- 
mata or of a diffuse fibrosis, or there may be an obliterating endarteritis 
of the coronary arteries. The symptoms may be those of failing com- 
pensation or of angina pectoris. 




Fig. 85. — A gumma in the subcutaneous tissue overlying the patella and surrounded by tertiary 

ulcers and scars. 

The arteries, especially those of the brain, often show obliterating 
ENDARTERITIS. They may also be the seat of small gummatous nodules 
in the adventitia (gummatous periarteritis). Syphilis is an important 
factor in the causation of aneurism. 

The Respiratory System. — The nose and larynx are favorite sites 
for the late manifestations of syphilis. In the nose ulcerating gummata 
often cause extensive destruction of bone, and great deformity. 

The EPIGLOTTIS and larynx may be the seat of diffuse infiltration or 
of circumscribed gummata, with ulceration, necrosis of the cartilages, de- 
formity and stenosis from cicatricial contracture, etc. The symptoms are 
those of hoarseness, aphonia, cough, stridor, dysphagia, etc. The pain, 
however, in contradistinction to that of tuberculous laryngitis, is usually 
slight or lacking. 

In the TRACHEA and large bronchi gummatous nodes, ulcers and 
cicatricial strictures occur rarely. 

Syphilis of the lungs is very rare and has little clinical importance. 
There may be scattered gummata ; a diffuse fibrosis beginning about the 
root of the hmg, or the so-called "white pneumonia" found in still-born 
syphilitic infants. 

The Genito-Urinary System. — Kidneys. — Acute nephritis sometimes 
develops in the secondary stage, and gummata are occasionally found. 



SYPHILIS 



445 



Syphilitic orchitis is rather common and occurs as an early tertiary 
symptom. The testicle proper is enlarged, hard, smooth and painless. 
The epididymis and vas are rarely involved. An associated hydrocele is 
not uncommon. 

The Nervous System. — Of all the various manifestations of tertiary 
syphilis those affecting the brain and cord are the most important. The 
lesions follow three chief types : 

(a) Distinct gummata, which are commoner in the brain than in the 
cord; are usually superficially placed, and which give the usual general 
and focal symptoms of a rather rapidly developing tumor. 

(b) Gummatous meningitis, involving chiefly either the pia or the 
dura mater. In the brain this thickening usually occurs at the base and 
tends to involve the cranial nerves, either by pressure or by extension of 
the inflammatory process to the nerve-trunks. 

(c) Syphilitic Arteritis. — This often results in occlusion of the 
lumen, and in softening or sclerosis of those areas in the brain or cord 
nourished by the affected artery. In the brain the middle cerebral, or 
some branch of it, is frequently involved. It is clear that in this last 
type of lesion the ^results of treatment must be much less satisfactory 
than in the other two. 

Parasyphilitic Affections. — This term has been applied to certain 
diseases not actually syphilitic, which nevertheless occur much more fre- 
quently in syphilitic subjects than in non-syphilitic. Among these are 
locomotor ataxia, paralytic dementia, and aneurism. They do not re- 
spond to anti-syphilitic treatment. 

HEREDITARY SYPHILIS 

Symptoms. — A large proportion of syphilitic pregnancies result 
either in abortion or in the child being still-born at term. Living chil- 
dren rarely show signs of syphilis at birth, but when present these 
consist of a skin eruption (papular, pustular or bullous), enlargement 
of the liver and spleen and grave malnutrition, and the infant ordi- 
narily dies within a few days. 

Early Symptoms. — The first evidences of syphilis usually appear be- 
tween the second and sixth week (rarely after three months) and cor- 
respond to the secondary manifestations of the acquired form. The 
earliest and most constant symptoms are ''snuffles" — a severe and per- 
sistent coryza — and hoarseness. About the same time a skin eruption, 
which is most often papular but which may be erythematous or eczema- 
tous, appears over the face, neck, buttocks, extremities, hands and feet. 
Fissures occur in the lips, at the angles of the mouth and about the 
anus, and mucous patches are seen on the mucous membranes and at the 
mucocutaneous margins. 

The constitutional symptoms become marked ; there are wasting, 
anemia, cachexia, slight fever, a loose, wrinkled, sallow skin, pinched 
features, digestive disturbances, hemorrhages, loss of hair and often, 
disturbances of the nails (onychia) and inflammation and possibly sepa- 



446 



DISEASES CAUSED BY ANIMAL PARASITES 



ration of the ends of the long bones, such as the femur, humerus, etc. 
(acute epiphysitis). These symptoms may last for a number of months 
and during this period the disease is highly infectious. 

Late Symptoms. — These correspond to the tertiary symptoms of ac- 
quired syphilis and do not always appear. They may develop at any 
time up to puberty or even later. They sometimes appear in children who 
have shown none of the early symptoms. The child is undersized, poorly 
nourished, wizened, and often mentally deficient. Puberty may be much 
delayed. The permanent teeth (second dentition) often show very char- 
acteristic abnormalities. The upper central incisors show a crescentic 




FiQ. 86. — Congenital sjrphilis, with depressed nasal bones and rhagades in the lips. The girl had also 
a general adenopathy and a syphilitic periostitis of the tibial. 

notch in the cutting edge and the teeth are dwarfed, wide apart and 
somewhat peg-shaped (Hutchinson's teeth). Gummatous lesions of the 
skin, mucous membranes, bones, periosteum, and viscera may occur as in 
the acquired form. Interstitial keratitis is the most frequent eye s^Tiip- 
tom. There may be dekfness. Enlargement of the spleen is very com- 
mon (see Fig. 86). 

Diagnosis of Syphilis. — In the primary and secondary stages this is 
usually not difficult. The possibility of extragenital chancre is to be borne 
in mind. The characteristic induration of the base and margins of the sore 
is present no matter where the lesion is situated. 

The manifestations of the secondary stage are usually readily rec- 
ognized by the association of sore throat, a general enlargement of the 
sul)cntaneons lymph-nodes, and skin eruptions, with the other symptoms. 



SYPHILIS 



447 



The diagnosis of late syphilis, however, when no satisfactory history 
is to be obtained, may be difficult or impossible. The skin, nose, throat, 
skull, shins, testicle, penis, etc., should be searched for scars, nodes or 
other evidences of old or recent syphilis. In women a history of re- 
peated miscarriages is very suggestive. Prompt and decided improve- 
ment under anti-syphilitic treatment may usually be looked upon as 
proof of the disease, although this test is not infallible. 

SYPHILIS 

The local lesions of syphilis, the chancre, eruptions, mucous patches, ' 
adenitis, etc., are so characteristic that they can ordinarily be recog- 
nized at once. The later lesions are more uncertain, especially those of 
cerebral syphilis. Two diagnostic procedures of the greatest value have 
recently come into general use. 

(1) Demonstration of the spirocheta pallida, the specific organ- 
ism. In all the lesions of syphilis, the organism can be demonstrated by 
appropriate measures. To obtain the spirocheta from exposed lesions, 
such as chancres, ulcers, or mucous patches, the lesion should be care- 
fully cleansed, and then curetted, and a drop of the serum exuding 
after the curettage examined. The specimen to be examined is dried in. 
the air and hardened in absolute alcohol for one hour, or fixed by heat 
like a blood-smear. Spirocheta pallida is a long, delicate, spirally-curved 
organism. The length varies from 4 to 14 microns. The fine spirals 
vary from 6 to 26 in number, and the organism is curved in its length 
as well as spirally. The stain now used is a modified Giemsa. 

Instead of staining the spirochete, the field may be stained by flooding 
the slide with india ink (a special ink is furnished by Eimer & Amend, 
of New York) and then washing and drying it. The spirochete will 
then stand out as a clear-shining white thread on a black background, 
the so-called dark field illumination. 

(2) Wassermann^s Reaction. — It has been shown that the blood 
serum of one animal species possesses the power of dissolving the red 
corpuscles of another species, and that this power can be intensified in 
any animal by repeated injections of an alien blood. This hemolysis 
is found to depend upon two factors, one of which is destroyed by heat- 
ing to 56° C. for half an hour, while the other survives. The latter 
is called the amboceptor because it apparently unites or binds the blood 
corpuscles and the third substance, the complement. If human red 
corpuscles be mixed with the serum of a rabbit which has been immunized 
by repeated injections of human blood, the human cells are promptly 
dissolved, i.e., hemolysis occurs. If, however, the rabbit serum be pre- 
viously heated to 56° C. hemolysis does not occur, because the comple- 
ment has been destroyed. But this complement can be resupplied by the 
addition of fresh serum of any kind, and the process of hemolysis will 
be completed. This mixture of red blood-cells, am])ocoptor, and comple- 
ment is known as a hemolytic system. 

In an exactly similar manner n bacteriolytic system can be built up. 



448 DISEASES CAUSED BY ANIMAL PARASITES 



An animal can be immunized by repeated injections of a given strain 
of bacteria. The blood-serum of the treated animal develops the power 
of binding and destroying the bacteria. This power depends on the 
two factors, amboceptor and complement, the latter destroyed by heating 
to 56° C. for one-half hour. The mixture of bacteria, amboceptor and 
complement in this case constitutes a bacteriolytic sj^stem, in which 
the complement can be destroyed and restored exactly as in the hemo- 
lytic system. 

Wassermann's test consists in mixing a hemolytic system devoid of 
complement, and a bacteriolytic system devoid of complement, and 
then adding just enough fresh serum to supply complement to one 
chain, but not to both. Under these conditions it is found that the com- 
plement will always be taken up first by the bacteriolytic system, and 
no hemolysis will occur. If, however, the bacteriolytic system is not 
properly constructed, that is, if serum does not contain the amboceptor 
fitted to the bacteria employed, the complement is not bound by this sys- 
tem, but is left to unite with the hemolytic amboceptor and hemolysis oc- 
curs. Hemolysis, therefore, becomes the test of the presence of the proper 
amboceptor in the bacteriolytic chain. In Wassermann's original scheme, 
sheep red cells and rabbit serum immunized to the sheep corpuscles were 
used for the hemolytic chain, the serum of the patient suspected of syphi- 
lis and an extract of syphilitic liver known to contain the spirocheta 
pallida as the bacteriolytic chain. When these four substances were 
mixed in a tube and complement in proper proportion added, if the sus- 
pected blood-serum really contained amboceptor (antibodies) as it would 
if the patient had syphilis, the complement would be taken up, there 
would be none left to complete the hemolj^tic chain and the corpuscles 
remained intact. If the patient's serum contained no amboceptor the 
complement served to complete the hemolytic chain and hemolysis became 
evident by the breaking up of the red cells and the coloring of the whole 
mixture red from the dissolved hemoglobin. When hemolysis did not 
occur, the red cells sank unharmed to the bottom of the tube and the 
mixture retained its normal clear straw color. 

Sheep red cells Emulsion of syphilitic liver 

Hem Complement Bacteri 



The principle of the test is indicated and the component parts sug- 
gested by the used of the words hem-o-lysis and bacteri-o-lysis. There is 
but one 0 (complement) available. If one word is completed, the other 
remains incomplete. If the patient is syphilitic, no hemolysis occurs and 
vice versa. A failure of hemolysis is, therefore, a positive reaction. 



lysis 

Rabbit serum immunized 
to sheep cells heated to 
56° C. 




lysis 



Patient's serum suspected of 
containing syphilitic antibodies 
and heated to 56° C. 



SYPHILIS 



449 



In the Noguchi modification, much used in this country, the arrange- 
ment is as follows: 

Human red cells Acetone insoluble residue of an 

alcohol-ether extract of normal 
heart muscle or liver. 
Complement 
Guinea-pig serum 

Rabbit serum immunized Patient's serum to be tested — 

to human blood — heated heated. 

Instead of the preparation from the liver of a syphilitic fetus (an 
organ rich in spirochetae) various substances have been used, solutions 
of lecithin, alcoholic extracts of liver, etc. 

In the Noguchi modification normal heart muscle or liver is extracted 
with alcohol, evaporated, the residuum dissolved in ether, evaporated, 
and the residuum treated with acetone. The part remaining undissolved 
in acetone is used. It is apparent that the substitution of such sub- 
stances in the test as well as the finding of the reaction in other condi- 
tions, such as leprosy and scleroderma, destroys its specific relation. 
These irregularities, however, do not seriously affect the value of the test. 

The test has been variously modified since its introduction, but the 
principle remains the same. So many factors are concerned that the 
utmost accuracy and care are required in carrying it out. Only those 
who have had months of training and experience with the test are 
capable of making reliable reports, but in such hands the test has become 
very valuable. It succeeds in more than 90 per cent, of early cases of 
syphilis and in varying proportions of others, depending chiefly on the 
vigor and duration of treatment. The cured patient will not react. 
In general paresis the percentage of positive reactions has reached 100 
in some series. 

The failure of a Wassermann test may result from various imperfec- 
tions in technique. Negative results are, therefore, not proof against the 
presence of syphilis unless confirmed by repeated trials. 

Positive Wassermann tests have been obtained in leprosy and occa- 
sionally in some other conditions, scleroderma, but the exceptions are not 
sufficient to affect the value of the test. 

Prognosis. — Except in the case of the congenital form, syphilis is 
rarely fatal in the early stages. The likelihood of severe tertiary manifes- 
tations is greatly diminished by thorough treatment, but cannot be alto- 
gether removed. Of these, those affecting the central nervous system are 
among the most frequent and important. 

Prophylaxis. — The problem of the prevention of syphilis is l)ound 
up with that of the efficient supervision and i'e<iulation of prostitution. 
Victims of the disease should be thoroughly informed as to its highly 
infectious nature and should be warned of the danger of transmitting it 
by sexual contact, kissing, etc., and by means of eating utensils, pipes, 
etc. Marriage should be forbidden for at least two years after all 
29 



450 DISEASES CAUSED BY ANIMAL PARASITES 



secondary symptoms have disappeared and until a prolonged course of 
treatment has been undergone. 

Treatment. — If any doubt as to the diagnosis exist treatment should 
be withheld until secondary symptoms appear. Mercury and potassium 
iodide are specifics; the former being specially useful in the secondary, 
the latter in the tertiary stage. Mercury may be administered by mouth, 
by inunction, by hypodermic injection or by fumigation. Gray powder 
(gr. 1), the protiodide (gr. 1/6-1/4), the bichloride (gr. 1/20-1/12) are 
the preparations chiefly used by mouth. They are given from three to 
six times a day. Daily inunctions of mercurial ointment (dr. 1) are 
an efficient but uncleanly method. Hypodermic injections have many 
advantages and have been growing in popularity. They should be given 
aseptically and deep into the muscles of the buttocks, to avoid the pos- 
sibility of abscess. For this purpose the salicylate of mercury, sus- 
pended by careful titration in albolene, one grain to 10 minims, is given 
in doses of one to two grains every four days. Whatever the method 
of administration, the mouth and teeth should be kept clean and in 
good order, to lessen the chance of salivation, and the treatment should 
be interrupted from time to time. In all, the treatment should be ex- 
tended over a period of some two years. The late manifestations of 
syphilis are treated most effectively by the combined use of mercury 
and the iodide of potassium. The latter is given in gradually increasing 
doses; beginning with five grains three times a day, and rising to 50 or 
more grains per dose. 

Treatment. — Ehrlich 's ' ' 606, " or salvarsan. Injections of this 
new drug have proven marvelously efficacious in causing the disappear- 
ance of the spirochete from the blood and tissues and bringing about 
the cure of local lesions. From 0.3 to 0.6 gm. is given by deep intra- 
muscular injection or intravenously. 

Various methods of preparing the drug for injection are employed. 
The following one is recommended. In a graduated, glass-stoppered 
bottle containing some glass beads the desired dose is put. Fifteen c.c. of 
hot sterile water are added, and the powder dissolved. Two c.c. of 4 per 
cent, sodium hydrate solution are next added and the mixture shaken. 
A heavy yellow precipitate is deposited. 

More sodium hydrate solution (%-l c.c.) is added till the precipitate 
is redissolved. The solution obtained is rather syrup-like and not clear. 
Sterile water is added to 20 c.c. and 10 c.c. are then injected deeply in 
each buttock. Care must be taken to avoid the sciatic nerve. The injec- 
tions are very painful and morphine is frequently required after them. 
Usually only one dose is given, but in severe cases the injection may be 
repeated after some days. The possibility of local abscess or sloughing^ 
from the injection must be recognized. 

To avoid the pain of intramuscular injection or for more immediate 
effect salvarsan may be given intravenously. The dose is prepared 
as above except that normal salt solution up to 200 c.c. is added. The 
perfectly-clear solution resulting is then introduced into the median- 
basilic vein by a needle just as the ordinary saline infusion. 



SMALL-POX 



451 



The use of salvarsan is contra-indicated in any patient having ad- 
vanced disease of the heart, arteries, kidneys, or nervous system. Par- 
ticular objection has been urged, because of bhnclness produced by injec- 
tions of the closely related atoxyl, to the use of salvarsan in cases of 
optic atrophy or neuritis. No ill results on the eye have thus far been 
recorded, but caution should be observed in its use under any of the 
conditions named. 

One injection of salvarsan, it was at first claimed, would cure the 
disease, but some cases have required 3 or 4 injections to produce any 
result and others are entirely refractory. Several weeks should elapse 
between the injections. 

After the use of salvarsan, systematic treatment with mercury and 
the iodides is advisable. 

SMALL-POX 
(Variola) 

Definition — Small-pox is an acute, highly contagious, infectious dis- 
ease, characterized by an abrupt invasion, marked constitutional dis- 
turbance and a skin eruption which passes through the stages of papule, 
vesicle and pustule. 

Etiology. — The disease has been well known for many centuries and, 
before the area of vaccination, constituted one of the commonest and most 
dreaded of the great pestilences. 

Distribution. — At the present day, although vastly less prevalent, it 
occurs in both endemic and epidemic forms over almost the whole 
world. Its prevalence in any district or country usually bears a direct, 
inverse relation to the care and thoroughness with which vaccination 
and isolation are carried out. 

Small-pox attacks all ages, even to the fetus in utero. It affects 
both sexes with equal frequency and is more prevalent during the colder 
months of the year. Negroes seem especially susceptible. Among 
aboriginal races the introduction of the disease has always worked 
frightful havoc. 

The EXCITING CAUSE is as yet unknown, in spite of a vast amount 
of effort expended in its investigation. It is certainly no one of the com- 
mon pyogenic bacteria present in the pustules. 

Although bacilli and cocci are regularly found in the cutaneous lesions 
of small-pox and sometimes also in the internal organs, these have all 
been shown to belong to the classes of cocci and bacilli commonly found 
in the skin and none of them has proven capable of producing the disease 
in animals. In the epithelial cells of the lesions of small-pox (and also 
vaccinia) are found certain small bodies of varying size and form. When 
small-pox is inoculated in monkeys the same small bodies are found in 
the lesions. Similarly they occur in the lesions produced by inoculating 
small-pox or vaccinia in the cornea of a rabbit, and can be traced throu,ii"h 
many successive inoculations from animal to animal. These small bodies 
are by some declared to bo protozoan parasites and the cause of the 



452 DISEASES CAUSED BY ANIMAL PARASITES 



disease. The varying forms have been arranged in series supposed to 
represent stages in the development of the parasite to which the name 
cytorrhyctes variola? has been given. Others declare these bodies to be 
cell-inclusions, the products of degeneration and of no etiological sig- 
nificance. The so-called parasites cannot be isolated or cultivated by 
any bacteriological methods. 

Yv^hatever its cause, the disease is one of the most highly contagious 
known. The contagious particles are given off from the skin in all 
stages of the eruption, but especially at the time of the drying of the 
crusts. They are probably present also in the expired air and in the 
various excretions. These particles are conveyed by the air, by fomites 
and through the medium of a third person. The virus is capable of 
remaining active for months and years in carpets, clothing, toys, etc. 

Malignant cases may be contracted from the very mildest ones. 

Immunity. — Susceptibility to the disease, in the unvaccinated, seems 
to be almost universal. One attack usually confers immunity for life. 
A second attack has, however, in rare instances, been observed. 

Morbid Anatomy. — The characteristic lesion is that of the eruption 
upon the skin and the mucous membrane of the mouth and air passages. 
Each papule consists of a central area of coagulation necrosis in the 
deep layer of the epidermis, surrounded by a zone of inflammation. By 
the gradual accumulation of serum and then of leukocytes, the papule 
becomes first a vesicle and then a pustule. Many of the pustules involve 
the true skin and these upon healing leave the familiar depressed scars 
or pocks. In severe cases parench;saiiatous changes in the heart muscle 
and in the liver and kidney are common. The hemorrhagic cases show 
extravasation of blood into the skin, mu(?ous membranes, meninges, vis- 
cera, etc. 

Symptoms. — The cases may be divided clinically into four types : the 
discrete, the confluent, the hemorrhagic or malignant, and varioloid. 

The period of incubation is commonly from ten to fourteen days. 
There are usually no prodromal symptoms. 

The Discrete Form. — The differences between the discrete and the 
confluent form are seen in the stage of eruption. In the stage of invasion 
the types usually cannot be distinguished. 

Stage of Invasion. — The disease begins suddenly, with one or more 
chills, vomiting, intense frontal headache and pains in the back and 
limbs, and a prompt rise of temperature to 103° or 104° P. All these 
symptoms are so constant and so severe as to be quite characteristic. The 
face is anxious and flushed, the pulse full and rapid and the respiration 
hurried. Prostration is marked. There may be delirium. In children 
the initial chill is often replaced by a convulsion. On the second or 
third day, in 10 or 15 per cent, of the cases, appear the so-called initial 
rashes. These are quite distinct from the true eruption and last 
but a day or two. They are usually either scarlatiniform or measly 
in character, but may be purpuric. They are confined to portions of 
trunk, thighs and upper arms. 



SMALL-POX 



453 



The fever on the second day is very high (104° to 106° F.) , but begins 
to fall on the third day and by the time of the appearance of the true 
rash is usually only slight. 

The RASH appears commonly upon the fourth day. It is first seen 
on the forehead and wrists and rapidly spreads over face, scalp, ex- 
tremities (including the hands and feet) and trunk. The eruption con- 
sists at first of small red spots Avhich almost immediately become raised 
(papules) and which have a peculiar, indurated, shot-like feel. They are 
present often to the number of several hundred and are least abundant 
over the trunk. The papules increase somewhat in size, and on the fifth 
or sixth day of the disease change to vesicles, which soon show a dis- 




FiG. 87. — The facial eruption of small-pox at the lieitrht of the disease. 
From the collection of Dr. S. D. Hubbard. 

tinct and characteristic depression at the center (umbilication) and a 
flattened top. All the vesicles at first are filled with clear serum, but in 
the course of a day or two (about the eighth day) they become pustules 
(see Figs. 87, 88), which quickly lose their umbilication and assume a 
rounded form; the spots first appearing being usually the ones first to 
become pustular. Around each pustule is an areola of hyperemia so that 
where the rash is abundant, as upon the face, the skin is greatly swollen, 
and is tense and very painful. In the course of two or three days the 
pustules break and begin to dry and by the fifteenth day are usually 
entirely replaced by yellowish crusts or scabs. These, in the course of a 
few days, separate and are cast off, leaving behind, in most cases, a dis- 
colored spot, but no cicatrix. Only those pustules which involve the true 
skin as well as the epidermis are followed by permanent scars or pocks. 



454 DISEASES CAUSED BY ANIMAL PAEASITES 



The emption is not confined to the skin. Simultaneously, there appear 
similar spots in the mucous membrane of the mouth, palate, pharj^nx and 
often as well in that of the larynx, trachea and bronchi. These spots, in- 
stead of becoming typical pustules, usually develop into small, superficial 
ulcers. 

With the appearance of the eruption the temperature falls, the severe 
constitutional symptoms subside and the patient remains comfortable 
until the developing pustules cause a second rise of temperature. Its 




Fig. 88. — The eruption of small-pox, showing marked umbilication and confluence of the vesicles. 
From the collection of Dr. S. D. Hubbard. 

height and the severity of the other symptoms depend directly upon the 
extent of the suppuration. The fever on the eighth or ninth day may reach 
104° or 105° F. Over the face, scalp and hands the pustules are usually 
abundant and the swelling, burning and itching correspondingly intense. 
There are also sore throat, dysphagia, hoarseness, cough, etc.. correspond- 
ing to the lesions of the mucous membranes. The temperature falls 
with the drying of the pustules and in moderate cases is normal before 
the end of the second week. AVith inistulation there is a well-marked 
leukocytosis. 

The Confluent Form. — The stage of invasion does not differ from that 



SMALL-POX 



455 



of the discrete form except in being rather more severe and often some- 
what shorter in duration. The rash appears on the third or fourth day, 
and is very profuse. The papules closely stud the skin of the face, scalp 
and extremities, and as they change into pustules many of them coalesce 
■ and form large suppurating areas (see Fig. 88). The face is greatly 
distorted by the swelling and hyperemia, the eyes are closed by edema, 
the suppurating areas emit a sickening odor and the pain, burning and 
itching are often intolerable. Over the trunk the pustules always remain 
discrete. The formation of numerous pustules and ulcers in the mucous 
membranes adds to the distress of the patient. The laryngeal symp- 
toms in particular are apt to be severe. The cervical lymph-nodes are 
greatly swollen and suppuration is not uncommon. There may be diarrhea. 

Corresponding to the extension of the suppuration the secondary 
fever is high, prolonged, and often irregular and septic in character. 
Delirium is common, prostration marked, the pulse grows progressively 
weaker and many of the patients die of exhaustion or of a complicating 
bronchopneumonia. In those that recover convalescence is slow and the 
cicatrization and pitting extensive. 

The Hemorrhagic or Malignant Form. — In this type the constitutional 
symptoms from the beginning are especially severe. The rash is atypical 
and often scanty and the patient may die before it is well developed. On 
the second or third day there appear petechige and larger hemorrhages into 
the skin and conjunctiva, followed by bleeding from the mucous mem- 
branes of the nose, mouth, stomach, intestines, kidneys, bronchi, uterus, 
etc. Extensive extravasation of the blood beneath the skin may fright- 
fully disfigure the face and body and justify the name black small- 
pox." The victim usually dies between the third and the sixth day. 
In some cases hemorrhages are not seen until bleeding occurs into 
the fully formed vesicles and pustules. 

Varioloid is the name given to the mild form of small-pox which occa- 
sionally develops in persons who have been vaccinated. The initial stage 
is less severe than in true variola and with the appearance of the papules, 
on the third or fourth day, the temperature becomes normal and does 
not again rise. The eruption is scanty and is confined chiefly to the 
face, scalp and hands. The scattered pustules heal rapidly and there is 
little or no scarring. The patient may at no time feel ill enough to go 
to bed, but it is important to remember that from such a mild case the 
most virulent type of small-pox may be contracted. 

Complications. — Severe laryngitis and bronchopneumonia are the 
most important complications. The former may excite a fatal edema of 
the glottis, or may result in necrosis of the cartilages. There may be 
pleurisy. Heart complications are rare. Parotitis, glossitis, membranous 
angina and otitis media are met with. Actual nephritis is not common. 
During the pustular stage, pyemia, septic arthritis and phlegmons may 
occur. 

Severe conjunctivitis is common and may lead to keratitis and corneal 
ulceration. 



456 



DISEASES CAUSED BY ANIMAL PARASITES 



During convalescence boils and abscesses often occur, and both local 
and multiple neuritis are met with. Inflammation of the substance of the 
brain ox cord may give rise to hemiplegia, aphasia, paraplegia, etc. 

Diagnosis. — Variola cannot be positively identified before the appear- 
ance of the eruption; but when the disease is prevalent every case of 
illness beginning abruptly with a chill and with intense headache and 
lumbar pain should be at once isolated. The initial rashes may in chil- 
dren be mistaken for those of measles or scarlet fever. Causes of hemor- 
rhagic small-pox present many difficulties. They may be confused with 
other purpuric conditions or may be fatal so early that only a most care- 
ful search will disclose the beginning eruption. In the stage of eruption 
the disease is usually easily recognized. In varicella the eruption is most 
abundant upon the trunk ; the papules have not the shot-like induration ; 
the vesicles are very superficial and are usually not umbilicated ; there is 
no surrounding zone of hyperemia; and few of the spots go on to pus- 
tulation. All stages of the eruption may be seen at one time. Moreover, 
the onset is usually not severe : the fever is slight, and the eruption 
appears upon the first or second day. The pustular eruption of syphilis 
may resemble that of small-pox, but the violent onset and the constitu- 
tional symptoms are lacking, and the distribution is different. 

Prognosis. — The mortality among unvaccinated persons varies in dif- 
ferent epidemics between 25 and 40 per cent. The death rate is highest 
in young children, drunkards and pregnant women. Hemorrhagic small- 
pox is regularly fatal, and the severe, confluent form is so in a majority 
of the cases. On the other hand, in varioloid {i.e., among the vaccinated) 
the death rate is not more than 1 or 2 per cent. 

Treatment. — Prophylaxis. — Ever^^ person who has been exposed to 
infection should be immediately vaccinated, as immunity can even then 
be acquired in time to prevent the attack. Whether vaccination after 
the disease has actually begun can mitigate its severitjT" is, however, 
doubtful. 

The patient should be rigidly isolated (best in a special hospital) and 
should remain so until all the crusts and scabs have disappeared. The 
greatest care is to be exercised in the disinfection of the bed linen, 
clothes, discharges, etc. (see Typhoid Fever), and in the proper disin- 
fection of the sick-room and its contents after convalescence. 

The treatment of the patient consists in very careful nursing and in 
meeting the symptoms as they arise. The diet should be fluid during 
the period of fever. The severe pain at the onset will often require mor- 
phine. The fever and the severe nervous symptoms are best met by cool 
baths or wet packs. The care of the eyes is very important — they should 
be kept clean and free of secretion by being bathed several times a day 
with a saturated solution of boracic acid. 

In the stage of pustulation the intense burning and itching of the 
face and hands may be somewhat relieved by the constant application of 
cold compresses wet with a solution of carbolic acid 1-100. Whether pit- 
ting be extensive or not will depend upon the depth of the pustules, and 



VACCINIA— VACCINATION 



457 



none of the many methods suggested for its prevention will avail in the 
severe confluent forms. As the pustules begin to dry the crusts should 
be kept moist or softened with vaseline or glycerine, to prevent the dis- 
semination of the contagium. Nothing is known that will control the 
profuse hemorrhages of the malignant form. 



VACCINIA— VACCINATION 

Definition. — Vaccinia or cow-pox is an infectious disease of cows, 
closely allied to small-pox, and marked by a similar eruption, material 
from which, when inoculated into man, produces a local infection and is 
followed by more or less complete immunity from the latter disease. The 
means of protection against small-pox (vaccination) was discovered by 
Jenner in 1796, and by its almost universal use has changed variola from 
the commonest and most dreaded of the great pestilences to an infre- 
quent and relatively harmless disease. 

Bacteriology of Vaccinia. — In spite of a vast amount of investigation, 
the active agent in vaccinia, as in small-pox, is entirely unknown. The 
vaccine lymph contains various micro-organisms, but none of them has yet 
been proved to be the cause of the disease. The same intracellular bodies 
described by some as the specific organism of small-pox ( cytorrhyctes vari- 
olas) have been found in the lesions of vaccinia, but, as in small-pox, 
their significance is questionable. 

Vaccination. — The virus or vaccine is obtained either directly from 
the vesicles of the calf (animal lymph) or from the vesicle of a vaccinated 
person (humanized lymph) . The former method is much to be preferred. 
The lymph is now almost altogether supplied from carefully managed 
vaccine farms where great care is taken to have it pure and free from 
contamination. Vaccine lymph is furnished either dried on small bone 
points or quills, or preserved in glycerine in sealed capillary tubes. 

Vaccination is done by carefully cleansing the skin with alcohol, 
scarifying an area % inch in diameter with a sterile needle or lancet and 
then well rubbing in the lymph and allowing it to dry before the clothes 
are adjusted. The spot should be kept clean and should t)e protected by 
a simple dressing or shield, to prevent contamination from scratching. 
The outer surface of the left arm, at the point of insertion of the deltoid 
tendon, is the most convenient place for vaccination. 

Symptoms. — On the third day after vaccination a small red papule 
appears at the site of inoculation. This increases in size and on the 
fifth or sixth day becomes a vesicle. By the eighth day the vesicle is 
fully developed, distinctly umbilicated, and the edge is indurated and 
reddened. By the tenth day the vesicle has become a pustule which is 
surrounded by a considerable zone of inflammation and hyperemia. In 
two or three days this begins to subside and by the fourteenth or fifteenth 
day the pustule has become a thick, firm scab, which in the course of a 
week or ten days drops off and leaves a rounded, depressed scar. As the 



458 



DISEASES CAUSED BY ANIMAL PARASITES 



vesicle develops there is apt to be much burning' and itching and some- 
times for several days a moderate fever. The axillary lymph-nodes on 
that side are usually enlarged and tender. 

Complications are rare and arise almost always from lack of cleanli- 
ness or from a debilitated state of health. Cellulitis, sloughing, axillary 
abscess and erysipelas are all occasionally met with. A few instances 
of the transmission of syphilis by the use of humanized vaccine are known. 
Tetanus is another very rare complication. Erythema multiforme, urti- 
caria, purpura, and other rashes are sometimes seen. It happens rarely 
thai; vaccination is followed not only by a local pustule, but by scattered 
pustules on various parts of the body, generalized vaccination. 

The IMMUNITY from small-pox furnished by vaccination varies much, 
both in its duration and in its completeness. In most persons there is 
complete protection for a number of years, but eventually the immunity 
lessens and if exposure occur, small-pox in its modified form (varioloid) 
may develop. Oftentimes, however, immunity lasts throughout life. 

Every child should be vaccinated when a few months old and 
should be revaccinated at intervals of eight or ten years and whenever 
an epidemic prevails. Persons who have been exposed to small-pox, if 
they be vaccinated immediately, can usually acquire immunity in time 
to prevent an attack. 

VARICELLA 
(Chicken-pox) 

Definition. — Varicella is an acute, contagious disease of childhood 
marked by a discrete, vesicular eruption and by mild constitutional 
symptoms. It has no relationship to small-pox. 

Etiology. — The disease occurs sporadically and in epidemics. It is 
contagious from the onset to the falling off of the crusts. Its specific 
g-erm is not known. Children between the ages of two. and ten years 
are chiefly affected. Immunity is usually procured by one attack. 

Morbid Anatomy. — The only characteristic lesions are those of the 
cutaneous eruption. 

Symptoms. — The period of incubation is quite regularly about two 
weeks. 

The disease usually begins with malaise and slight fever, but often 
the eruption is the first thing noticed. This appears on the first or second 
day as small red papules upon the back, face and scalp, which gradually 
spread over the rest of the body. The papules are scanty and widely scat- 
tered, and each is surrounded by a small red areola. Within a day or 
two most of the papules have developed into large, clear, superficial 
vesicles which are not umbilicated and which in another day or two begin 
to dry at the center and to form crusts. In the meantime other crops 
of pnpuh^s have appeared and it is characteristic of the disease to find 
frcsli i);ii)ules, vesicles and crusts all present at the same time. The erup- 
tion is never confluent and only exceptionally do the vesicles go on to 



TRYPANOSOMIASIS 



459 



pustulation. In the course of a week or two the crusts separate and 
fall off and as a rule leave no scar. A few vesicles are often seen 
in the mucous membrane of the mouth and occasionally in that of the 
larynx. The slight fever and other constitutional symptoms usually 
disappear in two or three days. Occasionally the temperature reaches 
103° or 104° F. During the eruption the itching is often very trouble- 
some, but otherwise the children usually feel quite well. Rarely the 
' eruption may be so severe and profuse as to threaten life. Erysipelas, 
nephritis, suppurative adenitis and gangrene of the skin are rare com- 
plications. The prognosis is almost invariably good. 

Diagnosis. — The mild onset, the early appearance of the rash, its 
scantiness, the absence of the shotty induration, of umbilication, and of 
pustulation, and especially the presence at the same time of all the stages 
of the eruption, serve to distinguish the disease from small-pox. Usually, 
too, there is a history of exposure. 

Treatment. — Isolation is not necessary unless there be other small 
children in the household. If instituted, it must be maintained until the 
skin is entirely clear of scales (about three weeks). Other children in 
the family should be kept from school for the same period. No treat- 
ment is needed as a rule, except the application of carbolated vaseline or 
some bland ointment to the skin to allay the itching. In young children 
care must be taken to prevent scratching. 

TRYPANOSOMIASIS 

Definition. — The morbid conditions caused by infection with trypano- 
somes, including protracted irregular fever, localized erythema or edema, 
anemia and emaciation, and terminating in the sleeping sickness. 

Etiology. — Within the last ten years infection of man with trypano- 
somes has been recognized. The parasites had been long known in the 
blood of horses and other mammals. Human infection has been found 
prevalent throughout the Congo basin and generally in Central Africa. 
The distribution of the disease is found to correspond to that of the tse-tse 
fly, which is now regarded as the intermediary host of the parasite. 
Europeans are rarely affected, while the native population is very sus- 
ceptible. 

Trypanosomes. — The parasite found in human blood, known as 
trypanosoma gambiensis, is an organism with a long, spindle-shaped body, 
rounded at one end, terminating at the other in a long flagellum, the 
continuation of a delicate undulating membrane which fringes the 
spindle-shaped body. The body contains a nucleus and several masses 
of pigment. The parasites have been found in the blood, cerebrospinal 
fluid, and lymphatic nodes. They are stained by the Romanowsky 
method. They are most easily found in the glands. In the blood they 
are few in number and are found only after centrifugation and verv^ care- 
ful examination. In the cerebrospinal fluid they appear only in the 
advanced stage of the disease known ns sleeping sickness. 



460 DISEASES CAUSED BY ANIMAL PARASITES 



Thus far artificial cultivation of the human trypanosome has not suc- 
ceeded, although the kindred organisms found in the rat and horse have 
been grown on suitable media. 

Transmission. — The infection is spread by the bite of the tse-tse fly, 
the organism being carried from the sick to the healthy. AA^hether the 
organism, like the malarial parasite, undergoes a certain development in 
the body of the intermediary host, or is merely carried by it, is not 
clearly established. By reason of the prevalence of the tse-tse flies 
along the shores of lakes and streams these regions are peculiarly 
dangerous. 

Morbid Anatomy. — The gross changes are those of anemia and emaci- 
ation. The spleen and liver may be enlarged, probably from previous 
malaria. A lymphocytic infiltration of the pia-arachnoid following the 
blood-vesels into the brain and cord is found microscopically. Similar 
perivascular infiltration is found throughout the body. 

Symptoms. — The period of incubation is about 20 days in experi- 
mental inoculation in monkeys; its exact duration in man is unkno^vn. 
The onset is slow and insidious ; months or even years may elapse before 
definite symptoms develop. Enlargement of the lymphatic nodes is 
an early sign, and there may be no other. Fever of variable height 
and duration occurs in most cases, with progressive anemia and ex- 
haustion. 

Sleeping Sickness. — Sooner or later the final phase of the disease 
is reached. Progressive feebleness, apathy, lethargy and an unconquer- 
able tendency to sleep terminate finally in coma and death. During this 
stage an irregular fever is present, headache and indefinite pains are 
complained of, tremor of hands or tongue may be noted, bed sores may 
develop. Patchy erythema or edema is sometimes seen. The blood may 
show a slight leukocytosis with lymphocytosis and secondary anemia. 
Trypanosomes are found on careful examination. 

Prognosis. — Recovery may occur in the early stage, but the sleeping 
sickness is regularly fatal. Towns have been wiped out and whole dis- 
tricts of Africa depopulated by this scourge. 

Treatment. — Prophylaxis. — The efl'orts at prevention follow the lines 
employed in relation to malaria. Isolation and protection of the infected 
persons to prevent infection of the flies cannot be satisfactorily prac- 
ticed because the infection is so wide-spread and so long latent. People 
entering infected districts should avoid the shores of lakes or streams 
which are the natural habitat of the tse-tse fl}^ and should protect 
themselves against its bite by screening houses and using mosquito 
netting. 

The most effective treatment of the disease consists in the intramus- 
cular injection of a 10 to 20 per cent, solution of atoxyl, a meta-arsenic- 
anilin compound, to the amount of one grain every third day, the dose 
being gradually increased. Much larger doses have been employed, but 
often with serious results. Blindness due to optic atrophy has repeatedly 
resulted from excessive doses. 



KALA-AZAR 



461 



KALA-AZAR 

(Tropical Splenomegaly, Dum-dum Fever, Black Sickness) 

Definition. — A chronic infective disease showing the presence in the 
internal organs of certain parasites, the Leishman-Donovan bodies, and 
characterized by chronic irregular fever, marked enlargement of liver 
and spleen, progressive anemia, exhaustion and death. 

Etiology. — The cause of the disease is infection with the Leishman- 
Donovan bodies, now regarded as forms of trypanosomes and given the 
name of herpetomonas Leger, Two forms of the parasite are known, one 
as it is found in the internal organs or blood of man, the other obtained 
by growth on culture media. In the first form the organism is a small 
oval or rounded body 2-4 micra in diameter, having two chromatin 
masses, one larger, the nucleus, and a smaller nucleolus. The parasites 
multiply by fission, the nucleus and nucleolus dividing before the body. 
They are regularly intracellular, being found especially in the endo- 
thelial cells of blood- and lymph- vessels, and most abundantly in the 
spleen and liver. 

The cultural forms are much larger, 12 to 20 micra in length, and 
flagellated, but without the undulating membrane of the trj^panosoma 
gambiensis. 

It is assumed that the parasite is transmitted from man to man by 
the bite of some blood-sucking insect or tick, but as yet this is not proven. 
The disease is endemic in Southern Asia, especially India, and Northern 
and Southern Africa. Local epidemics are known. 

Morbid Anatomy. — The spleen and liver are both enlarged, the 
spleen sometimes enormously. In the cells of both organs the parasites 
are found in large numbers. The liver has a brown or mottled section. 
The bone marrow also shows the parasites in great numbers. The lym- 
phatic nodes are generally enlarged. Intestinal ulcers are common. The 
blood and all the viscera may show the parasites. 

Symptoms. — The incubation period is less than ten days. The onset 
is marked by high fever, possibly a chill, which continues from two 
to six weeks, and is accompanied by marked enlargement of liver and 
spleen. A period of apyrexia follows, to be succeeded by fever and splenic 
and hepatic swelling. These periods of fever and apyrexia continue in- 
definitely. Anemia, emaciation and finally edema of the legs or ascites 
appear. At the end of a year or two the patient dies of exhaustion or of 
intercurrent dysentery, pneumonia, or phthisis. 

The blood shows a secondary anemia with a marked hypoleukocytosis ; 
the ratio of red to white cells may be 2,000-4,000 to one. There is a rela- 
tive lymphocytosis. The parasite may be demonstrated by Leishman's 
or Giemsa's stain. 

Diagnosis. — Malaria must be excluded by repeated examination for 
the Plasmodia and the trial of quinine. Other tropical fevers, such as 
trypanosomiasis, can be differentiated only by the demonstration of the 
parasites in the blood or in material obtained by puncture of liver or 



462 



DISEASES CAUSED BY TREMATODES 



following this procedure. The parasites have been demonstrated in 
smears from excised lymph-nodes (Cochran). 

Treatment has, therefore, been unsatisfactory. Atoxyl may be given 
in 2-grain doses every third day. Change to a healthful climate, rest and 
good food are indicated. 

OTHER PARASITIC PROTOZOA 

A number of other varieties of protozoa have, at times, been found in 
the human body. (1) Cercomonas intestinalis, a pear-shaped flagellate^ 
found in the feces. (2) Trichomonas intestinalis, a similar pear-shaped 
organism endowed with ameboid movement. (3) Balantidium coli, an 
ovoid body, 7 to 10 micra in length, provided with ciliae, also found in 
the feces, especially in diarrheal conditions. (4) Trichomonas vaginalis, 
similar to the intestinal form, but smaller. Whether any of these varieties 
is of pathogenic importance has not been established. 

DISEASES DUE TO ANIMAL PARASITES OTHER THAN 
PROTOZOA-METAZOA 

The animal parasites of man other than protozoa are sometimes 
grouped under the broad title of metazoa. They include a number of 
diverse groups, some but distantly related to the others, and these groups 
are constantly being added to. The common metazoan parasites, however, 
are of these varieties. 

(1) Trematoda (literally holed, or having holes), leaf -shaped organ- 
isms, having an intestine, but no anus, and one or tvs^o suckers ; parasitic 
in the lungs, liver, intestine ; blood flukes. 

(2) Cestoda (the cestus, banded), long, segmented organisms, with 
suckers, but no intestine ; adults, parasitic in the intestine, the larvae 
elsewhere ; tape-worms. 

(3) Nematoda. (Thread-like organisms.) Intestine present; para- 
sitic in intestines, muscles and lymphatics, including common round 
worms, filaria and trichinella spiralis. 

DISEASES CAUSED BY TREMATODES 

DISTOMATOSIS : FLUKE INFECTIONS 

Definition. — Infection by a trematode. The parasite may lodge in the 
lungs, liver, intestine, or veins of any part of the body. The resulting 
condition is designated as pulmonary, hepatic, intestinal or venal disto- 
matosis. 

Etiology. — The life-cycle of the parasites is complicated, and may in- 
volve two or more generations living outside of man. The parasites are 
hermaphrodites. Direct infection from man to man appears possible. 

The disease is almost unknown in the ITnited States, but very common 
in Japan and China, whence practically all our knowledge of it is derived. 



DISTOMATOSIS : FLUKE INFECTIONS 



463 



Morbid Anatomy. — In the lungs thick-walled cavities filled with 
muco-pus, blood and ova, and communicating with the bronchi, are 
formed. The parasites may be found in them. 

Symptoms. — Pulmonary Distomatosis. — A chronic cough with an 
abundant brownish or reddish muco-purulent expectoration is the chief 
symptom. Blood is commonly present, and hemorrhages not infrequent. 



4# 




Fig 89. — Bilharzia hematobia, or Schistosomum hematobium, showing female lying within the male. 

(Copied from Braun.) 

The condition suggests tuberculosis. The diagnosis is made by finding 
the characteristic ova in the unstained sputum. 

Parasite. — The paragonimus Westermani, as it is now called, is a 
plump oval or pyriform fiuke, 8 to 16 mm. by 4 to 8 mm. and about 2 to 
4 mm. in thickness. 

The eggs are oval bodies, measuring 50 by 90 micra. with an opercu- 
lum or lid at one extremity. They are usually found in numbers. 

Hepatic Distomatosis — Liver Fluke. — The parasitic is known as fas- 
ciola hepatica, and is a small trematode, measuring from 20 to 30 mm. by 



464 



DISEASES CAUSED BY NEMATODES 



8 to 13 mm. The eggs are yellowish-brown, oval bodies, 140 by 70 micra. 
The liver is enlarged and tender; janndice or ascites may develop. The 
ova are found in the stools. 

Other liver flukes, bearing the name of Opistorchis sinensis, have been 
described. 

Venal Distomatosis. Blood Fluke — Bilharzia Hematobia. — In this 
condition the flukes lodge in the portal vein, or the veins of the intestine 
or bladder wall. Infection is brought about through drinking contam- 
inated water. The disease is common in the tropical and sub-tropical 
climates, especially in Egypt. It has been observed in Cuba and Porto 
Eico, and in a few instances in the United States. 

Morbid Anatomy. — The ova, not the parasites themselves, are the 
active agents in the disease. From the portal or other veins where the 
worm is lodged the ova make their way into the walls of the intestine, 
bladder or rectum. Here they are grouped in masses, showing as whitish 
specks, surrounded by inflammatory thickening. Ulcers may develop or 
a diffuse thickening with papillary outgrowths. 

Symptoms. — Two forms of the disease are recognized, according as 
the bladder or rectum is most involved. In the former hematuria is 
present, possibly cystitis, pyelitis, or pyelonephrosis. In the latter diar- 
rhea with discharge of blood and pus. 

Diagnosis — Microscopic examination reveals the presence of the char- 
acteristic eggs in the urine or feces. The ova are spindle-shaped with a 
small spine projecting from one side or extremity. They measure 0.12 
to 0.19 mm. by 0.05 to 0.07 mm. Within the egg is a ciliated embryo 
which is set free when the eggs are placed in water and thus becomes 
the means of spreading infection. 

The Parasites. — The male Bilharzia is 4 to 15 mm. long by 1 mm. 
in breadth (see Fig. 89). The female is filiform, from 15 to 20 mm. in 
length and lies with a canal in the body of the male. 

Treatment. — Male-fern or santonin may be given, but with doubtful 
effect. The treatment must be supportive and symptomatic. 

DISEASES CAUSED BY NEMATODES 
ASCARIASIS— ROUND-WORM OR EEL-WORM INFECTION 

Parasite. — Ascaris lumbricoides resembles the common earth-worm 
(angle-worm), but is longer and more pointed at the extremities. The 
male measures from 15 to 20 cm. in length, the female from 20 to 40 cm., 
the diameter varying from 3 to 5 mm. (see Fig. 90). Their habitat is 
the small intestine. The eggs develop into embrs^os which grow into the 
adult forms. No intermediate host is required (see Fig. 91). 

Etiology. — Infection with the round-Avorm is the most frequent par- 
asitic infection of man. Children most often harbor these worms, but 
they may be found at any age. The infection is carried by contaminated 
water or food. The house-fly may be the means of spreading contagion, 
particularly in country districts where privies are used. 



ASCARIASIS— ROUND- OR EEL-WORM INFECTION 465 



Symptoms. — In the great majority of cases no symptoms are excited. 
In other cases, especially if many worms are present, all manner of dis- 
turbances of the stomach, intestine, and nervous system may be pro- 
duced. Loss of appetite, nausea, or vomiting, colicky pains, diarrhea or 
constipation, headache, vertigo, convulsions, chorea, epilepsy and the like 
have all been attributed to round-worm infection. Particular significance 
is commonly attributed to fretfulness and irritability, picking at the nose, 
dark rings under the eyes, grinding of the teeth, or offensive breath. 
Most probably these symptoms are due to improper feeding rather than 
to the presence of the round worms. 



The most pronounced symptoms of as.^ariasis are due to the habit of 
the worm of wandering from the small intestine into other parts. They 
may block the bile-ducts and produce jaundice; crawling into the 
stomach they may excite persistent vomiting and be ejected per orem; 
They may block the larynx and cause death by suffocation ; or they may 
pass through the Eustachian tube and escape through the ear. 

Diagnosis. — The appearance of the worms in the feces, or in vomitus, 
etc., is conclusive. They are often seen in the stools, without symptoms 
of any kind. The eggs are easily recognized in feces. They are oval 
bodies, measuring 50 to 70 micra in length and 40 to 50 micra in breadth, 
with a thick transparent shell usually covered by an albuminous coat. 
The body of the egg is unsegmented. 



Prophylaxis. — The essential points are the proper disposal of fecal 
material, and personal cleanliness. In cities in this country ascaris 
infections are becoming infrequent except in the tenement house popu- 
lation. 

Treatment. — Santonin, usually combined with an equal amount of 
calomel, is given in divided doses, one-half to one grain every half hour 
to a total of from 2 to 5 grains for an adult. The dose should be re- 
peated from time to time so hmg as ova appear in the feces. 



Parasite. — Oxyuris vermicularis, the pin-worm, seat-worm or thread- 
worm, is a small, white nematode, from 8 to 5 mm. (male) to 10 mm. 
(female) in length. The adult worms inhabit the small intestine, where 
they copulate. The fertilized female Avanders to the cecum or colon. 




Fig. 90. — Ascaris lumbricoides. i to I natural size. 




Fig. 91. — Ovum of ascaris lumbricoides, showing shell and envelope. X 400. 



OXYURIASIS— PIN-WORM INFECTION 



30 



466 



DISEASES CAUSED BY NEMATODES 



Eggs are passed, and often the female worms in numbers wander from the 
anus, and are found in the skin, in the vagina or bladder. 

Etiology. — As the female worms containing ova wander from the 
anus and the eggs are also passed in the feces, infection may be direct 
or by means of contaminated water or vegetables. Autoinfection is 
doubtless frequent and serves to perpetuate the condition. 

Oxyuris infections are extremely common in children, rare in adults. 

Symptoms. — Inflammation of the anus caused by scratching to re- 
lieve the itching produced by the presence of the parasites, restlessness 
and sleeplessness, since the itching is worse at night, are characteristic. 
All or any of the indefinite symptoms narrated under ascariasis may be 
attributed to the oxyuris. 

In children the oxyuris frequently lodges in the appendix and may be 
a cause of appendicitis (Cecil and Bulkley). 

Diagnosis. — The worms, looking exactly like active little white 
threads, can often be seen in the feces, in the creases of the anus or on 



the adjacent parts (see Fig. 92). Eggs may be found on microscopic 
examination of the feces. The eggs are oval, measuring 50 by 20 micra, 
and embryos can often be seen in them, distinguishing them from the 
unsegmented ova of ascaris lumbricoides. 

Treatment. — Santonin and calomel, as for ascaris, should be given to 
remove the young worms from the small intestine. Infusion of gentian, 
thymol or betanaphthol may be used for the same purpose. 

To clear the colon and rectum, injections of various kinds are used. 
Infusion of quassia, lime water, or strong salt water or salt in milk may 
be used. Weak carbolic acid and bichloride of mercury solutions have 
been used, but the possibility of poisoning should forbid their employ- 
ment. The enemata should be repeated daily for several times, then at 
intervals till all signs of infection have disappeared. Both the parasites 
and ova should be sought for. 



Parasite. — Three stages of the parasite, trichinella spiralis, are to 
be distinguished: (1) The adult worms living in the small intestine; the 
males 1.4 to 1.6 mm. in length, the females 3.0 to 4.0 mm. The males 




Fig. 92. — Oxyuris vermicularis. Natural size. 



TRICHINIASIS 



TRICHINIASIS 



467 



die shortly after copulation. The females remain in the intestine or 
bore into its lymphatic spaces, and being viviparous, there deposit their 
young, about 1,500 for each female worm. (2) The embryos, microscopic, 
thread-like organisms, grow to 100 micra in length, pass into the blood 
stream from the lymph spaces, and are thus distributed throughout the 
body. The embryos reach the muscles in from 10 days to 2 weeks fol- 
lowing infection. (3) Having reached the muscles the embryos coil 
themselves up into round or oval bodies and become surrounded by a 
fibrous capsule, thus forming the encysted larvae, the infecting stage of 
the parasite. When meat containing such larvae (the so-called measles) is 
eaten, the capsule is dissolved off, the embryo set free in the intestine, 
and the chain of reproduction renewed. 




Fig. 93. — Patient with trichiniasis, showing the pufEness of the eyelids. 

The larvae may be found in the meat of a number of animals, such as 
rats, dogs and cats, but for man the pig is the source of infection. Hogs 
are infected through eating the flesh of rats containing the larvae, and 
the rats are probably infected from other rats or from the refuse of 
abattoirs. 

The larvae are killed by thorough cooking, so tliat the disease is com- 
mon only among people who, like the Gormnns or Australians, habitually 
eat raw pork. It regularly occurs in localized outbreaks, when the meat 
of a trichinous hog has been consumed by a family or group of persons. 
"Whole villages have been poisoned in this way. Germany now maintains 
a costly microscopic inspection of all hogs slaughtered in her abattoirs 
in the effort to prevent^such occurrences. 

In America the disease is met with in sporadic cases, occasionally in 



468 DISEASES CAUSED BY NEMATODES 



the several members of one famil}-. The incidence and severity of the 
disease seem to depend on the amount of the infected pork eaten. 

The disease becomes more frequent in this country as the number 
of people accustomed to eating raw pork increases. 

Symptoms. — The period of incubation is usually from 10 days to 
2 weeks. Diarrhea with abdominal pains may occur during this period, 
but is usually absent. The invasion of the disease corresponds to the 
lodgment of the embryos in the muscles of the victim. A puffiness 
(edema) of the eyelids and face m.ay be noted at the outset (see Fig. 93). 
Then follow fever, low or high, pains in the muscles, sometimes exquisite 
tenderness, especially in the arms and legs, profuse sweats, loss of appe- 
tite, nausea or vomiting, constipation and headache. 

Except for the edema of the face, muscular pains and tenderness, the 
onset closely resembles typhoid fever. All these symptoms continue for 



/ 7, s ^ 'j- 6 7 y I // 




Fig. 94. — Typhoid-like fever of trichinosis. 



from 2 to 7 weeks, according to the severity of the infection. The 
patients may die of exhaustion, but for the most part recover slowly. 

The fever of trichinosis is of the continuous type with remissions 
usually more marked than those of typhoid (see Fig. 9-4). It may be 
high or low. It falls by lysis. The spleen is enlarged and in some 
instances there is a roseola which cannot be distinguished from the 
rash of typhoid fever. Headache and mental dulness are usually 
pronounced. The muscle pains and tenderness are often absent or very 
mild. 

Blood. — A leukocytosis of 15,000 or more is present in most cases 
and the differential count shows an eosinophilia varying from 5 to 50 
per cent., or even more. 

Diagnosis. — The resemblance to typhoid fever is very close. The puf- 
finess of the eyelids and face is very suggestive. The leukocytosis and 
eosinophilia are almost conclusive. The final proof lies in finding the 
embryos either in the blood or muscle. T. C. Janeway has shown that 



TRICHINIASIS 



469 



the embryos may be found in the blood by the method experimentally 
developed by Staiibli. Several eabic centimeters of the blood (2-10) 
are drawn from a vein by a hypodermic needle, laked with from 10 to 
15 parts of 3 per cent, acetic acid, centrifuged, and the embryos sought 
in the sediment. It is not yet known how reliable the method is in man. 
If it fails, a fragment of any muscle, the deltoid, biceps, or gastrocnemius^ 
for example, may be excised under cocaine, hardened, sectioned, stained 
and examined microscopically. A characteristic myositis with many 
eosinophile cells is found here and there, and in some of the areas the 
encysted larva will be discovered. If few in number, it may require 
the examination of many sections to demonstrate the larvse. 

Prognosis. — The disease is fatal in about 5 per cent, of cases. The 
milder cases regularly recover. 

Prophylaxis. — Thorough cooking of all pork or pork products will 
kill the parasites. Microscopic examination of the flesh of all slaughtered 
hogs and the rejection of all infected carcasses have greatly reduced the 
prevalence of the disease in Germany, but many local outbreaks and 
sporadic cases still develop, because the meat is often eaten raw. 

Treatment. — By the time the disease comes under observation the 
embryos have already left the intestine and are lodged in the muscles 
and other tissues. Purgatives and anthelmintics, therefore, are of no 
avail. The treatment must be wholly symptomatic and supportive. Hot 
baths or morphine may be used to relieve severe muscular pains. Atro- 
pine will check the profuse sweating. 

UNCINARIASIS OR HOOK-WORM DISEASE 
Parasite. — Two distinct species of uncinaria are known, an Old World 
and a New World hook-worm. The Old World form, the ankylostomum 
duodenale, or uncinaria cluodenalis, is commonly found in Europe, Asia, 
Africa and Australia. It is but 8 to 18 mm. in length. The head is 
armed with a number of sharp teeth, by which it fixes itself in the 
intestinal mucous membrane. The species found in this country, uncin- 
aria americana (Stiles), is shorter, 7 to 11 mm., and presents certain 
differences in the minute anatomy of the head (see Fig. 95). 

The eggs of the two species are oval, measuring 60 or 70 micra by 
40 (see Fig. 96). They are usually somewhat segmented and may con- 
tain fully developed embryos. No intermediary host is required. 

Both parasites inhabit the small intestine, more often jejunum or ileum 
than duodenum. 

Etiology. — The eggs of uncinaria passed in the feces (see Fig. 96) 
undergo development in moist earth or water. Infection may take place 
by one of two routes. 

(a) By ingestion of the ova or embryos in contaminated water or 
food. 

(b) By passage of the embryos through the skin into the circulation, 
and thus to the lungs, then up the air tubes to the pharynx, and so into 
the stomach and intestine. Roundabout as this route is, it has been 



470 



DISEASES CAUSED BY NEMATODES 



demonstrated by Loos and others, and infection through the skin doubt- 
less plays a considerable part among tropical people wearing no shoes 
and in constant contact with the soil. 

Uncinariasis has long been known throughout the tropics, and in parts 
of Europe, especially Italy and Switzerland. Recently it has been 
shown to be very prevalent in the Southern States, Cuba and Porto Eico. 
Ninety per cent, of the inhabitants of Port Rico and of certain districts 
in the South harbor these parasites. Children suffer particularly. Rural 
communities, farmers, brick-makers, tunnel workers and others in close 
contact with the soil are especially liable. The infection is rare in the 
Northern States, and particularly hi cities. 

Symptoms. — (1) There may be no symptoms, and the eggs may be 
found in casual examination of the feces. 




Fig. 95. — Uncinaria americana. Upper figure, female X 63; lower figure, male X 63. The white lines 
on the dark square show the natural size. (International Clinics, Vol. IV, Series 20, page 142.) 

(2) Anemia, with pallor, palpitation, etc., marks the majority of cases. 
In some instances the anemia is profound, and the blood picture is that 
of pernicious anemia. 

(3) The dirt-eaters of the South, with their stunted growth, anemia, 
emaciation, protuberant abdomens, edema, or ascites, and physical or 
mental lethargy, are types of severe chronic infection with the ankyl- 
ostomum. 

The Blood. — Anemia, varying from a mild secondary anemia to 
typical pernicious anemia, is present. Leukocytosis is unusual. Eosino- 
philia is common, but may be absent in chronic cases. 

Prognosis. — The infection in its milder forms is curable. The severer 
cases are often fatal. Thirty per cent, of the deaths in Porto Rico have 
been attributed to uncinariasis. The prevalence of the infection in a 
considerable portion of the poorer population of the Southern States, 



UNCINARIASIS OR HOOK-WORM DISEASE 471 



Porto Rico, Cuba and tropical countries renders it of vast economic 
importance. 

Diagnosis. — In badly infected districts severe anemia or the clinical 
picture of dirt-eating are suggestive. In all cases of severe anemia, the 
feces should be examined for the ova, or after an anthelmintic for the 
worms, which are often present in numbers. (See Fig. 97.) 

Prophylaxis. — The proper disposal of fecal material is the essential 
measure. In cities an adequate sewage system, in the country proper 
privies, in mines the pail system should be provided. 

Treatment. — Thymol or male-fern is administered after the prepara- 
tory measures given under tape-worm infection. Thymol is given in 2 





Fig. 96. — Uncinaria americana. Ova and larva magnified about 1500 times. (International Clinics, 

Vol. Ill, Series 20, page 143.) 

dram doses in capsules, the dose repeated in two hours, and followed 
by a purge. Male-fern may be used as for tape- worm. 

FILARIASIS 

A considerable number of filaria have been found in man during recent 
years, but of these only two are sufficiently common to make them of 
practical importance : the filaria Bancrofti and filaria loa. 

FILARIA BANCROFTI 
The parent worms are delicate, transparent, hair-like organisms, trans- 
versely striated, 50 to 100 mm. in length. Two sexes are recognized and 
are regularly found together, often closely intertwined, in lymphatic 
varices or in lymph-nodes. They are viviparous. The larva?, 300 to 400 
micra in length, are found in the circulating blood. (See Fig. 98.) They 
are provided with a sheath and a sharply pointed tail. They appear in 
the peripheral circulation during the night, but by day crowd into the 



472 



DISEASES CAUSED BY NEMATODES 



lungs, heart and internal organs. If the patient sleeps by day and is 
about at night, the periodicity of the organisms is reversed and they 
appear in the peripheral blood by day. The larvae are harmless. Accord- 
ing to Manson, the symptoms of filariasis are produced by the blocking 
of lymphatics by the adult worms or the immature products of con- 
ception, whatever these may be. 

The filarial larvae dra\\Ti into the stomach of a mosquito undergo a 
certain development in the muscles of that insect and then make their 
way to the proboscis, after 20 or 30 days, and thence again reach the 
body of man and become mature parasites. The larval forms can survive 
for a time in water, and contaminated water may, therefore, be a means 
of infection. 




Fig. 97. — A photomicrograph showing the ovum of Ankylostomum duodenale in the feces. X 500. 
From the collection of Dr. Walter B. James. 

These parasites are found in all tropical and sub-tropical countries, 
especially Africa, as far north as Spain and Charleston, S. C, and as 
far south as Australia. 

Symptoms. — These depend upon blocking of lymphatics or lymph- 
nodes by the parasites or their products and include lymphangitis, 
lymphatic varices, enlargements of lymph-nodes, abscesses, chylous ef- 
fusions into the peritoneum or tunica vaginalis, chyluria, and elephan- 
tiasis. Of these, chyluria and elephantiasis are most important. 

Chyluria. — This condition results from the rupture of lymphatic 
varices in the walls of the bladder or some other part of the urinary tract. 
The urine becomes milky white or pinkish, if blood as well as chyle is 
present (hematochyluria) . 



FILARTA BANCROFTI 



473 



On standing the urine separates into three strata, an upper creamy 
layer, a reddish sediment, and an intervening milky fluid, usually con- 
taining a coagulum. The sediment shows red blood-cells, lymphocytes, 
granular fatty matter, epithelium, and usually filari^e. The middle and 
upper layers contain much granular fatty matter, and larger oil globules. 
The fat may be dissolved out by ether. 

Chyluria comes and goes for months or years ; when protracted, de- 
bility and anemia are produced. Retention of urine may result from 
stoppage by blood clots. 

Elephantiasis. — Brawny thickening of the skin and subcutaneous 





Fig. 98. — Filaria Bancroft! in the blood. From the collef'tion of Dr. Walter B. James. 

tissues due to lymphatic obstruction (elephantiasis) is now known to 
be a late consequence of filarial infection. The lower extremities, the 
scrotum, or penis are most often involved. The enlargement of the 
feet and legs may be enormous, or the scrotum and penis may form 
huge tumors. Attacks of lymphangitis, dermatitis and cellulitis, accom- 
panied by fever (elephantoid fever), occur from time to time. With 
each attack the enlargement of the affected parts increases. The skin 
and subcutaneous tissues become greatly thickened, dense, and do not 
pit on pressure. All inflammatory symptoms subside, but the patients 
suffer from the weight and hindrance of the enlargement or tumors. 
Scrotal tumors of 10 to 15 pounds are common, and one of 224 pounds 



474 



DISEASES CAUSED BY NEMATODES 



has been reported. The enlargements are permanent. Filaria cannot be 
found in the tissues, but there are many reasons for believing filaria to 
be the cause. 

Prophylaxis consists in protection against mosquitoes. 

Treatment. — For chyluria rest with elevation of the hips, to lessen 
pressure on the broken lymphatics, is the only measure of value. For ele- 
phantiasis elastic bandaging, elevation and massage may be tried. Surgi- 
cal removal of large tumors may be required. 

FILARIA LOA 

This thread worm closely resembles filaria Bancrofti. The adult male 
measures from 30 to 34 mni. in length, the female somewhat less. They 
are both marked by numerous rounded, translucent bosses on the cuticle. 
They are found in the subcutaneous tissue of any part of the body, es- 
pecially of the extremities or of the eje. The microfilariae can hardly be 
distinguished from those of f. Bancrofti, except that they are found in 
the blood by day, and are disposed in rather uncouth lines instead of the 
graceful loops or circles assumed by the microfilaria B, ]\Ianson says 
that one suggests the awkward, angular writing of a schoolboy, the 
other the easy flowing strokes of a skilled penman. 

F. loa is widely distributed through tropical West Africa; it has 
rarely been seen in the United States. 

Symptoms. — F. loa may cause pricking, itching or pain and irrita- 
tion with transient local edema of any part of the body. It seems to 
prefer the loose connective tissue of the conjunctiva or eyelid and there 
may cause irritation and congestion. 

Treatment. — F. loa has often been removed from the eye by incision 
and traction. 

DRACONTIASIS 

Parasite. — Draeunculus medinensis or filaria dracuncula, Guinea- 
worm, is a remarkable parasite found in Southern Asia, tropical Africa 
and some parts of Brazil. It is found in many of the lower animals. 

Nothing definite is kno^^Ti of the male worm. The female attains a 
length varying from 30 cm. to 120 cm., and a diameter of 1.5 mm. 
The body is cylindrical and milky white. It is mostly occupied by the 
uterus filled with coiled-up embryos. 

The impregnated female is found in the connective tissue, nearly 
always in the lower extremities, but possibly in the arms or head. Bor- 
ing downward she bursts through the skin, producing a small ulcer on 
the leg, from which milky fluid is discharged. On examination the 
fluid is found full of active embryos, measuring from 0.50 to 0.75 mm. 
in length. 

Cj^clops quadricornis, a minute fresh-water eopepod or crustacean, is 
the intermediary host. The infection is, therefore, water-borne. The 
life-span of the female draeunculus is calculated at one year. 

Symptoms. — Ulcers discharging a milky fluid are found at the point 



DKACOXTIASIS 



475 



of exit. If the parasite dies in the subcutaneous tissue an abscess may be 
caused, or the body of the worm may become calcified and be palpable as 
a cord beneath the skin. 

Treatment. — When emptied of her embryos the worm is absorbed or 
can easily be extracted. Until that time, normally 15 to 20 days, extraction 
is difficult. Repeated douching of the ulcer with cold water causes 
contraction of the worm and hastens the evacuation of the embryos. 

The parasite, if projecting, may be injected with bichloride of mer- 
cury, 1 to 1,000, which kills her, so that extraction can be practiced after 
24 hours. 

If the parasite does not project, but can be felt under the skin, she 
may be killed by injecting a few drops of the solution at several points 
about her, and then left to be absorbed or cut down upon and extracted. 

DISEASES CAUSED BY CESTODES 
Parasite. — Tape-worms are formed of a head (scolex) and detachable 
segments (proglottides) ; on the scolex form sucking disks by which it 
attaches itself, and in some cases a rostellum with booklets. The segments 
may number hundreds, each containing a branched uterus from which ova 
in great numbers are discharged. Each ovum contains a minute embryo 
which under the conditions found in the intestines of various animals, 
cattle, pigs, fish (or even man) is set free, makes its way from the intes- 
tine to the muscles or viscera of the intermediary host and there lodges 
and becomes encapsulated, producing a cyst-like growth, variously 
called measles, cysticercus or hydatids. In this state they lie dormant 
indefinitely. When muscle or meat containing these cysts is ingested by 
man the embryo is set free in the intestine, effects lodgment and grows 
into the adult worm. Thus the common intestinal infection is produced. 
In certain rare instances man becomes the intermediary host with result- 
ing infection with the bladder forms, cysticercus or hydatid disease. 

INTESTINAL INFECTIONS 

A considerable variety of tape-worms has been found in the human 
intestine, but of the number only four are common. 

(1) Tenia mediocanellata (see Fig. 99, A, B, C). The beef tape- 
worm. Cattle are the intermediary hosts and man is infected by eating 
raw meat containing the embryos. This is the form most often found in 
the United States. The average lengih of the worm is 4 to 10 meters, 
though some are much longer. The head is roughly cubical and measures 
1 to 2 mm. in diameter. It has a rostellum but no hooks. The uterus, 
which forms the conspicuous feature of each segment, sends out from 20 
to 25 branches, each of which breaks up into a number of smaller tubes. 
The many divisions of the uterus constitute the chief differential of the 
segments from those of t. solium. 

The eggs are spherical in form, 30 to 40 micra in diameter, with a 
distinct shell. 



476 



DISEASES CAUSED BY CESTODES 



(2) Tenia solium (see Fig. 100, A, B, C). The pork tape-worm. The 
pig is the intermediary host, and man is infected by eating raw or poorly 
cooked pork. This worm is, therefore, common in Europe, but is very 
infrequently seen in the United States, unless in immigrants. It has an 
average length of 2 or 3 meters. The head is rounded, about 1 mm. in 
diameter, armed with a rostellum and a double circle of hooks. The ripe 
segments are very like those of tenia saginata, but the lateral branches 
of the uterus number only 10 to 12 and its finer divisions are not so 
numerous. The spherical eggs so closeh^ resemble those of t. saginata 
that they cannot be distinguished microscopically. 




Fig. 99. — Tenia mediocanellata or saginata. A, head and segments, natural size; B, head, showing 
sucking disks but no booklets, X 7; C, proglottis, showing branched uterus and sexual pore, X 7. 

(3) Dibothriocephalus latus. Fish tape-worm. Fish are the inter- 
mediary hosts, especially pike, perch or salmon. It is, therefore, common 
in lake regions. It is frequently met with throughout Europe, particu- 
larly on the shores of the Baltic and in Northern Italy; in the United 
States it is rare. The adult worm is from 2 to 9 meters in length, made 
up of many segments (3,000-4,000). These are commonly broader than 
they are long. The head is oval, 2-3 mm. in length, without booklets, 
and with a lateral groove instead of suckers. The divisions of the uterus 
are few and simple. The eggs are oval, 45 mm. by 70 mm., of brown 
color, and in some cases show a small operculum or lid. 

(4) Hymenolepsis nana. The rat tape-worm. The smallest tape- 
worm known for man is but 5 to 45 mm. in length, witli from 100 to 
200 small segments (see Fig. 101). The head has a rostellum and many 



INTESTINAL INFECTIONS 



477 



hooklets. The segments show a single, unbranched uterus. The eggs 
are round, from 50 to 40 micra in diameter, having a double shell, the 
inner shell showing polar projections with filamentous appendages (see 
Fig. 102). 

The frequency of this parasite has only lately been recognized. It 
is common in Sicily, 10 per cent, of the children being said to be infected. 
A number of cases have been reported in the United States. 

In the rat the eggs of this worm develop in the villi of the intestine, 
and the larvae from this seat easily reach the intestine. Man is pre- 




FiG. 100. — Taenia solium. A, head, with hooklets and sucking disks, X 10; B, ovum, X TOO; C, proglot- 
tides, X .25. 

sumably infected through eating food infected with ova from the feces 
of rats, and a like cycle must be assumed. 

Habitat. — The tenia? regularly lodge in the upper part of the small 
intestine. 

Symptoms. — In the great majority of cases tape-worm infection pro- 
duces no definite symptoms, until segments of the worm are passed and 
observed in the feces. In nervous women great distress may be produced 
by the knowledge of this evidence of infection. In other cases vague 
digestive disturbcinces are complained of. The excessive appetite com- 
monly believed to be excited by tape-worm infection is wholly legendary. 
Since microscopic examination of the feces is now generally practiced, 
the ova of tape-woi-ms are often found unexpectedly. 



478 



DISEASES CAUSED BY CESTODES 



Severe anemia may be caused by tape-worm infection, particularly 
b}^ the dibothriocephalus latus. For this reason the feces of all anemic 
patients should be examined for oya. An eosinophilia is regularly 
present in the blood. 

Diagnosis. — The appearance of segments or ova in the feces is the only 
reliable evidence. The different varieties of tape-worm are distinguished 
by details of the structure of the ova, segments, or heads of the worms. 
Eosinophilia is always suggestive. 




Fig. 101. — Hymenolepis nana, enlarged. (International Clinics, Vol. IV, Series 19, page 255.) 



Prophylaxis. — The segments of tape-worms should be burned. In- 
fected beef or pork should be rejected in the abattoirs. The cystieerci^ 
if present in numbers, show plainly, especially in the muscles of the 
tongue and neck. All meat or fish should be thoroughly cooked. 

Treatment. — The intestine is emptied by a limited diet for two days 
or more and the use of mild purgatives. Fasting for 24 hours is some- 
times enjoined. Then one of the anthelmintics is given in full dose and 
followed in 2 or 3 hours by a full dose of castor oil. Of the many anthel- 




FiG. 102. — Ova of Hymenolepis nana. (International Clinics, Vol. IV, Series 19, page 260.) 

mintics the following are preferred : Extract of male-fern in doses of 1 
to 2 drams. Kousso, 5 to 7 drams in an infusion or tablets or capsules. 
Kamala, 1 to 2 drams in syrup or cinnamon water. Pumpkin seeds, 3 
or 4 ounces macerated for 12 hours, and the resulting liquor given. 

The Avorm should be passed into warm water, as contact with cold 
leads to violent contraction with possible breaking of the chain. The 
segments should be collected and washed and the head sought. .Often 
it escapes detection, even when passed. Two or three months must then 
elapse before cure is assured by non-reappearance of segments. If seg- 
ments reappear, treatment must be repeated. 



VISCERAL INFECTIONS 



479 



VISCERAL INFECTIONS 
As already pointed out, if the ova of certain tape-worms are taken into 
the human stomach, the embryos there set free pass through the intestinal 
wall, make their way through the lymph- channels to the circulation and 
are distributed to all parts of the body. Lodging in the subcutaneous 
tissues, muscles or the viscera they form the cyst-like structures char- 
acteristic of the larval stage. These cysts may grow to some size and 
present symptoms as tumors. This chain of events takes place in the 
case of two known tape-worms, the tenia solium and the tenia echino- 
coceus. 

CYSTICERCUS CELLULOS^E 

The ova of tenia solium may reach the human stomach by ingestion, 
the patient himself or some one in close contact with him harboring the 
mature worm and passing the ova in the feces, or mature segments con- 
taining ova may wander from the intestine into the stomach or may be 
drawn into the stomach by prolonged vomiting. Cystic tumors contain- 
ing the embryos may then form in any part of the body. The most 
frequent seats of lodgment are the subcutaneous tissue, the muscles, the 
brain or the eye. In the subcutaneous tissue and muscles they form 
multiple small, movable tumors. If few, no symptoms are excited. If 
many, there may be pain and stiffness. 

The small cysts are most often casually discovered in the course of 
post-mortem examination. The diagnosis has occasionally been made 
during life by the excision of one of the nodules and its microscopic 
examination. In the brain the cysticercus, if lodged in the motor area, 
may give rise to irritation and produce attacks resembling Jacksonian 
epilepsy, or general convulsions. In the ventricles they may grow to con- 
siderable size. Lodged in the floor of the fourth ventricle the cysts may 
cause diabetes, persistent vomiting, or respiratory paralysis. The diag- 
nosis is practically never made during life. Before careful inspection 
of all meats was practiced in Germany, Virchow is said to have found 
cysticercus in the brain of one out of every 30 post-mortem subjects ; after 
the establishment of inspection, the number fell to one in 280. Brain 
cysticerci are very rarely observed in this country even in post-mortem 
work. 

In the eye the cysticercus forms a tumor which may be recognized. 

ECHINOCOCCUS DISEASE. HYDATID CYST 

Tenia Echinococcus. — The mature parasite, a small tape-worm, is 
normally found in the intestine of the dog, fox, wolf or jackal. The dog is 
naturallj^ the agent in human infection. In Iceland 28 per cent, of the 
dogs are infected, in Australia, 40 to 50 per cent., in America but very 
few. The worm is one of the smallest cestodes, being from 3 to 6 mm. 
in length. The minute head bears four suckers, a rostellum and a 
double row of from 28 to 50 booklets. The body consists of only 3 or 
4 segments, which, however, contain great iinnibcrs of eggs. The ova 



480 



DISEASES CAUSED BY CESTODES 



are from 30 to 36 micra in diameter and have a thin striated shell. 
Through contaminated drinking-water or vegetables, or by direct contact 
with an infected dog, the ova may reach the human stomach. The shell 
is then dissolved, the embryo set free, and making its way through the 
intestinal wall passes into the portal vein and so reaches the liver, or 
reaching the general circulation through the lymph-channels it may be 
carried to any part of the body and lodge in the lungs, brain, spleen 
or any of the other viscera. 

The importance of the echinococcus infection rests upon the remark- 
able evolution which the embryo undergoes when lodged in a favorable 
site, such as the liver. One month after infection the parasite is repre- 
sented by a minute cyst, perhaps 1 mm. in diameter, surrounded by a 
fibrous sheath. Gradually this cyst enlarges and its wall becomes differ- 
entiated into two distinct layers, an outer laminated fibrous sheath 
derived from the connective tissues of the host and an inner germinal 
layer representing the parasite. The cavity contains clear fluid. As 
growth continues the cyst continually enlarges, its fibrous sheath thickens 
and from the germinal layer new cysts are budded off, forming the so- 
called daughter cysts, each of w^hieh is filled with fluid in which float 
a number of scolices (the head-segments of the adult worm) armed with 
their characteristic booklets. The number of daughter cysts produced 
is apparently without limit. In course of time these daughter cysts 
become free in the fluid of the primary cyst, and may by their friction 
upon one another give rise to the peculiar fremitus sometimes detected 
in hydatid cysts. Also some of the daughter cysts may degenerate and 
the scolices and booklets be set free in the fluid of the primary cyst. In 
this manner a hydatid cyst may grow to form an enormous cystic tumor 
surrounded by a dense fibrous capsule, the inner part of which is lami- 
nated in a manner which renders it pathognomonic of the disease. The 
fluid of hyatid cysts is clear or slightly yellow in color, neutral or faintly 
acid, of a specific gravity 1010 to 1015, containing traces of sodium 
chloride, glucose, inosite, leucin, cholesterin and albumin. The fluid also 
regularly shows under the microscope the characteristic scolices and 
booklets, and crystals of cholesterin. The scolices are small oval or 
spherical bodies 0.2 to 0.3 mm. in diameter. The rostellum and double 
row of booklets may be protruded so as to be readily visible or may be 
retracted so as to be seen only when one looks directly into the rostellar 
opening. The presence of scolices and booklets is diagnostic. 

The evolution thus described gives rise to one great cyst containing 
many smaller ones, the so-called endogenous development. In rare in- 
stances some of the secondary cysts penetrate the primary capsule and 
undergo evolution outside of it, giving rise to an exogenous development, 
the so-called multilocular echinococcus. 

An echinococcus cyst may die, its contents become inspissated into a 
pasty mass or calcified. If secondary infection with pyogenic organisms 
takes place at any time, suppuration develops and the cyst becomes an 
abscess. In rare instances the cyst ruptures and discharges its contents 



ECHINOCOCCUS DISEASE 



481 



into the bronchi, the gall ducts, the intestine, the urinary passages, or 
even the inferior vena cava. 

Symptoms. — An echinococcus cyst is a slow-growing tumor. In the 
liver it causes discomfort or actual pain, indefinite gastric disturbances, 
and possibly jaundice. It presents itself as an enlargement of the liver, 
steadily progressive. A tumor may be outlined, and if superficial the 
peculiar fremitus caused by impact of the daughter cysts upon one an- 
other may be felt. The tumor is tense and fluctuation can rarely be de- 
termined. 

Diagnosis. — Hydatid cysts are most often recognized at operation. 
If the tiuid be aspirated or discharged, the finding of booklets or scolices 
is pathognomonic. Even apart from these, the composition is suggestive, 
the crystals of cholesterin and the presence of sugar being important. 
Where only remnants of the cyst are obtained, the laminated chitinous 
membrane is characteristic. 

Hydatid cysts of the spleen or peritoneum will present similar symp- 
toms and signs. In the lung the tumors can be recognized only by the 
discharge of booklets or scolices in the sputum. The blood may show 
leukocytosis, and an eosinophilia is regularly present. A complement- 
fixation analogous to the Wassermann reaction has been demonstrated, 
employing echinococcus fluid as antigen. 

Prophylaxis. — The dog, being the host of the adult worm, should be 
avoided, particularly in districts where infection is common. The dogs 
obtain their infection from eating the flesh of sheep, cattle, or hogs suf- 
fering from hydatid diseases. Dogs should not be allowed to feed on the 
refuse of abattoirs. 

Treatment. — The cysts must be opened and drained, and the lining 
membrane removed. If suppuration has taken place, the cyst must be 
treated as an abscess. 



31 



X 



DISEASES OF THE NERVOUS SYSTEM 

DISEASES OF THE NERVES 
NEURITIS 

Definition. — An inflammation of a nerve. Two forms are recognized, 
local, involving a single nerve, and general or multiple neuritis, in which, 
many nerves are affected. 

Etiology. — The local form is due (1) to traumatism, such as 
blows, or lacerations, the pressure of instruments or tumors, or (2) to 
exposure to cold and wet, or (3) extension of inflammation from 
adjacent parts, as the facial nerve is invqlved in caries of the temporal 
bone. Multiple neuritis may be caused (1) by the toxins of acute 
infectious diseases, especially typhoid fever or diphtheria, (2) by poisons 
such as lead, arsenic, mercury, phosphorus, alcohol, or illuminating gas, 
(3) by cachectic states, such as occur in cancer or tuberculosis, (4) by 
exposure to cold and wet. The cause of the endemic neuritis kno^vn as 
beri-beri is as yet unknown. 

Morbid Anatomy. — The lesions are sometimes interstitial, especially 
in the localized form, or parenchymatous in multiple neuritis, or both. 
In the INTERSTITIAL TYPE the connective tissue between the nerve fibrils 
is swollen, edematous, and possibly infiltrated with small round cells. 
The nerve-fibers show some signs of degeneration. In the parenchy- 
matous TYPE the nerve fibrils undergo fatty degeneration and are 
broken up into globules which stain black with osmic acid. Both the 
axis-cylinders and their myelin sheaths are destroyed. Later the fatty 
droplets are absorbed and only the connective-tissue framework of the 
nerve remains. Some of the changes of the interstitial type are always 
found in this. 

Symptoms. — Localized Neuritis. — Sensory disturbances usually 
constitute the chief feature, pain in the territory of the nerve, deep 
and boring in character, tingling and numbness. The ner\"e itself is 
tender and may rarely be felt as a thickened cord. Tactile sense may 
be normal, numbed or lost. Motor disturbances are shown in weakness 
or loss of power in the tributary muscles. Atrophy follows. Twitchings 
or contractures of the affected muscles are not uncommon. Trophic 
changes may appear, the skin becoming shiny, edema appearing and 
the nails becoming ridged and brittle. The reaction of degeneration may 
develop in the paralyzed muscles, or the response to the current may 
be normal. Sncli localized neuritis is best shown after dislocation of 
the shoulder, or injuries of the ulna, at the elbow. The duration of 
symptoms varies from a few days to months. 
482 



DISEASES OF THE NERVES 



483 



Multiple Neuritis.— Ac it^e Primary Type. — The disease is ushered 
in by fever, headache, pains in the limbs and back, all the symptoms 
of an acute infection. Sensory symptoms (except pains in the limbs) 
are lacking. Loss of power is noted in the leg's and gradually extends 
upwards, as in Landry's paralysis. The arms, trunk, and even face 
may be involved. Foot-drop or wrist-drop and loss of reflexes develop. 

The disease may be fatal in a few days or the patients recover after 
weeks or months. Recovery may not be complete. 

The disease is with difficulty distinguished from Landry's paralysis 
or acute anterior poliomyelitis. A definite etiological factor is important. 
The presence of sensory disturbances and tenderness of the nerves are 
important. The reaction of degeneration may be present. 

Subacute Secondary Type. — This condition follows poisoning by 
lead, arsenic, or alcohol and the like. Either the sensory or the motor 
symptoms of a neuritis may be most prominent, although both are 
present. In lead poisoning the loss of power is most striking; in 
arsenical or alcoholic poisoning the sensory symptoms are marked. The 
symptoms of a localized neuritis are present, but not limited to one 
nerve. The affection is bilateral and symmetrical, both legs to the 
knees or the arms to the elbows being involved. Rarely are the thighs 
or shoulders affected. Pain, tingling, numbness and tenderness over the 
main nerve-trunks, especially in the calves of the legs, are prominent 
in alcoholic or arsenical cases. In lead poisoning, on the other hand, 
paralysis is marked often without sensory symptoms. Lead palsy most 
often affects the wrist, producing wrist-drop, i.e., weakness or disability 
in extending the wrist, when the hands are held prone with arms stretched 
forward. Alcoholic or arsenical neuritis, on the other hand, commonly 
involves the leg, producing foot-drop and the steppage gait. The flexors 
of the ankle being weak the toes drop when attempt is made to lift 
the foot as in walking. To meet the difficulty, the knee is raised 
higher than usual and the foot is thrown outward and forward in a 
half circle, coming down on the pavement with a flap like a flail. The 
tendon reflexes (patellar or wrist) are diminished or lost. 

Trophic symptoms are often present. Bed-sores may develop. 
Atrophy of muscles is marked. The reaction of degeneration is regularly 
present. In the alcoholic cases persistent delirium with hallucinations 
of sight or hearing may appear. A low fever is occasionally seen, and 
the patients become greatly emaciated and debilitated. Stupor with 
loss of control of the sphincters or even convulsions may develop. The 
condition is most often seen in women who drink moderately but steadily. 

The course of the disease varies greatly, but is regularly favorable. 
After weeks or months the symptoms grndunlly siil)si{l(» and power 
returns. Death is possi])le in very severe cnses, especially in the alcoholic 
type. 

The neurons are regenerated from their centers (ganglion cells) in 
the anterior horns of the spinal cord or on the posterior roots. 

The reaction of degeneration is present in the affected muscles. 



484 



DISEASES OF THE NERVOUS SYSTEM 



Earadic excitability is impaired or lost. A stronger galvanic current 
than usual is required to cause contraction and the action of the poles 
is reversed so that A C C > K C C, i.e., the anode closure contraction is 
greater than the cathode closure contraction. 

Diagnosis. — The symptoms and local signs of multiple neuritis are 
characteristic. The reaction of degeneration is important. In some 
cases without sensory symptoms and little tenderness of the nerves it 
may be difficult to decide whether the nerve-trunks or the anterior horns 
of the spinal cord are affected. 

From locomotor ataxia careful examination shows marked differences. 
There is weakness, but not ataxia. The steppage gait is very different 
from the gait of tabes. Lightning pains are absent. Romberg's sign 
and pupillary changes are missing. 

In alcoholic cases the delirium often causes the neuritis to be over- 
looked. The combination of wrist- or foot-drop and tenderness of the 
peripheral nerves with delirium and hallucinations is characteristic. 

Treatment. — Rest in bed and careful nursing are most important. 
In severe cases an air or water bed is desirable. Alcohol, if the cause, 
should be gradually withdrawn. Local hot applications may relieve the 
pain. A lotion of m-cnthol and chloral oii of each, in alcohol and 
camphor water (each gi), may be used for the same purpose. 

After the acute stage, gentle rubbing, massage, and electricity are 
indicated. Strychnine is given in full doses. 

NEUROMATA 

Tumors of nerve-fibers may be composed of nerve tissue, even includ- 
ing ganglion cells, the true neuromata, or may consist of fibrous tissue, 
the false neuromata. 

True neuromata are exceedingly rare, but occur in the thoracic or 
abdominal cavities on branches of the sympathetic system. 

False neuromata are common. They occur early in life and are often 
congenital. They may be found on any of the cranial or spinal nerves, 
and vary in size from minute dots to tumors several inches in diameter. 

Histologically, they consist of fibrous tissue, derived either from the 
epineurium, in which case they may hardly involve the nerve-fibers, or 
the endoneurium, when the nerve-fibers are scattered through or stretched 
over the tumor. 

The growths may be single or occur in thousands. 

Solitary Neuromata. — Pain, paresthesia, and muscular spasm in the 
territory of the affected nerve may be caused by a single neuroma. Loss 
of sensation or power is rare. Pressure upon the tumor excites or in- 
tensifies the pain, while pressure on the nerve-trunk proximal to the 
tumor relieves it. Neuromata are movable with the nerxe from side to 
side, but not in its length. Excision may be required. 

Multiple neuromata occur under several different conditions, (a) 
Plexiform neuromata, in which multiple tumors occur on all the branches 



DISEASES OF THE CEREBRAL NERVES 



485 



of a nerve, are most often seen on the head or neck, (b) Tubercula 
dolorosa, in which multiple fender and painful tumors are found on the 
terminal branches of cutaneous nerves, (c) General neurofibromatosis 
or von Reichlinghausen's disease — in which numerous sessile or pedun- 
culated tumors of the nerves are found scattered all over the body. Nevi 
and skin pigmentation are often associated. Nervous symptoms are rare. 
The location of the nodules and their histological examination establish 
the diagnosis. 

DISEASES OF THE CEREBRAL NERVES 

Disturbances of the cerebral or cranial nerves may be either functional 
or organic. The functional disturbances are seen particularly in neuras- 
thenia or hysteria and are evidenced by intensified, diminished or per- 
verted function without organic lesion. Organic disturbances are de- 
pendent upon lesions either in the nuclei of origin of the nerves, in 
the course of the nerves through the cranial cavity or its walls, or 
in their peripheral distribution. The lesions are varied and the dis- 
turbances in question are considered in various diseases, such as tumors of 
the brain, affections of the cerebral vessels, meningitis, fractures of the 
cranial bones, otitis media, and the like. Certain features of the affec- 
tions of the cerebral nerves can, however, be best treated by consider- 
ing them separately and individually. 

THE OLFACTORY NERVE AND TRACT 

The olfactory centers of the brain are localized in the hippocampal 
gyrus and the adjoining convolutions. From these the olfactory tracts 
pass forward on the under surface of the frontal lobe to the olfactory 
bulb, which lies on the cribriform plate of the ethmoid bone. From the 
bulb a series of twenty or more fine nerve-bundles pass through the 
cribriform plate and are distributed to the upper part of the nasal 
septum and to the outer walls of the nasal fossa as far down as the 
lower border of the superior turbinate bone. The remaining portions of 
the nasal mucous membrane are supplied with sensory branches from 
the fifth nerve, but at present no part in olfactory sensation is attrib- 
uted to them. 

Anosmia, loss of the sense of smell, may be congenital, from lack of 
development of the olfactory nerves, or acquired. The acquired form 
may be purely functional, as in hysteria or neurasthenia., or organic. 
The organic lesions most frequently causing anosmia are diseases of the 
nasal mucous meml)rane, such as acute or chronic rhinitis, or diseases 
of the nasal bones, fractures of the l)ase of the cranium involving the an- 
terior fossa, or pressure upon the olfactory bulb or tracts by hemorrhagic 
or inflammatory exudates or tumors of the brain. Temporary loss of 
the sense of smell is common after attacks of influenza. Paralysis of the 
fifth nerve, causing cessation of nasal secretions, may indirectly cause 
anosmia. 



486 



DISEASES OF THE NERVOUS SYSTEM 



Hyperosmia, abnormal acuteness of the sense of smell, is usually func- 
tional. 

Parosmia, a perverted sense of smell or olfaeton^ hallucination, is 
rare, but may arise from irritation of the olfactory nerves caused by the 
pressure of tumors, or may occur as an epileptic aura, and has been ob- 
served in locomotor ataxia. 

The treatment of these conditions must be that of the underlying 
cause. 

OPTIC NERVE AND TRACT 

The primary neurons of the optic tract lie, for the most part, in the 
retina. Thence the nerve-fibers pass backward to the chiasm, where 
the internal fibers pass to the other eye, the external to the optic tract 
of the same side, while the middle fibers cross into the opposite tract 
and are distributed to the external geniculate body, the pulvinar of 




Fig. 103. — The paths of the nerve-fibers in the optic chiasm. The fibers from the outer halves 
of the retinae do not cross and he in the corresponding outer portion of the chiasm; the fibers from the 
inner halves decussate in the central part of the chiasm. 

the optic thalamus and the superior corpus quadrigeminum. These 
centers are in turn connected by a secondary neurone system with the 
cortex of the cuneus and adjacent regions. (See Fig. 103.) 

Examination of the eyes, particularly of the retina, is of the 
utmost value in many cases of systemic disease. 

Retinitis. — Notable changes in the retina are common in Bright 's 
disease, syphilis, leukemia and anemia. These changes include (1) 
cloudiness of the retina, as a whole, due to serous exudation, (2) blur- 
ring of the disk for the same reason, (3) engorgement of the veins, and 
possibly (4) hemorrhages. These hemorrhages show as dots or larger 
areas, red or almost black in color, depending upon their age. V^ith 
them are frequently associated (5) white patches due to degeneration or 
atrophy of the retinal elements caused by previous hemorrhages. 

Several types of retinitis are recognizable, (a) Albuminuric. In 
from 15 to 25% of cases of chronic nephritis, especially of the inter- 
stitial type, retinal changes are present. Vision fails as the retinitis 
advances. The retinal cloudiness, hemorrhages and white spots are 



OPTIC NERVE AND TRACT 



487 



usually all present. The changes in the disk are commonly less 
marked, but they may be extreme, and the condition may then hardly 
be distinguishable from "choked disk" due to increased intracranial 
pressure. 

Retinitis in Bright 's disease is always of grave import. Recovery 
may follow, but if the changes are marked death ordinarily follows 
within six months or a year. 

(b) Syphilitic. Retinitis is common in both hereditary and ac- 
quired syphilis. Chorioiditis and often iritis are associated with it. It 
is marked by congestion and haziness of the disk, scattered gray or 
white spots, often fringed with pigment and circumscribed exudations, 
along the lines of the larger blood-vessels, forming white lines. 

(c) Diabetic. This may be the same as the albuminuric type, or it 
may be marked by small, bright, white spots above the macula and 
punctate hemorrhages, but without swelling or haziness of optic nerve 
or retina. 

(d) Leukemic. Marked swelling of the disk and retina and many 
hemorrhages are present. The vessels are large and tortuous, the 
blood pale. The fundus is pale and white or yellow spots of exuda- 
tion, foci of leukocytic infiltration, are seen. 

Papillitis (choked disk). — The disk is swollen, prominent, white or 
gray in color, and often presents white spots and hemorrhages. The 
retinal veins are distended and tortuous, and both veins and arteries 
appear broken or interrupted in their course. The retina is swollen, 
hazy, and presents white patches and hemorrhages. Increased intra- 
cranial pressure is the usual explanation, especially that produced by 
tumor of the brain, but in some cases no adequate cause can be found. 

Atrophy of the optic nerve is either primary or secondary to papil- 
litis. The optic disk appears paler than normal, the color varying 
from, gray to greenish-white. The center is sunken and the lamina 
cribrosa may appear. The arteries appear narrow. Primary atrophy 
occurs in tabes, or paralytic dementia, and rarely in multiple sclerosis. 
Secondary atrophy follows optic neuritis (papillitis), embolism of the 
central artery, glaucoma and retinitis pigmentosa. 

Amblyopia and amaurosis without retinal changes occur in a 
variety of conditions, uremia, diabetes, malaria, anemia, poisoning by 
methyl-alcohol, quinine and the like. Hysteria or neurasthenia may 
cause these conditions. 

Hemianopsia. — A lesion of either optic nerve anterior to the chiasm 
will produce blindness in the corresponding eye. A lesion of the chiasm 
itself so situated as to involve the fibers pnssinu' to the nasal half of 
each eye will cause insensitiveness of those parts, with the result that 
the outer or temporal half of the visual field is not appreciated. This 
condition is called bitemporal hemianopsia. 

A lesion of either optic tract behind the chiasm produces loss of 
the same half of the visual field in both eyes, or bilateral homonymous 
hemianopsia. 



488 



DISEASES OF THE NERVOUS SYSTEM 



Hemianopsia is therefore of importance in the localization of intra- 
cranial lesions. It may, however, be produced by functional disturb- 
ances, such as megrim, hysteria or neurasthenia. 

THE OCULOMOTOR, TROCHLEAR AND ABDUCENS NERVES 

(Third, Fourth and Sixth Nerves) 

The nuclei of origin of the third and fourth nerves lie in the floor 
of the aqueduct of Sylvius;, of the sixth in the floor of the fourth ven- 
tricle. The third emerges on the inner aspect of the crus just behind 
the optic chiasm. The fourth winds around the crus and appears on 
its outer side ; the sixth emerges from the groove between pons and 
medulla. All three pass forward in the outer wall of the cavernous 
sinus, through the sphenoidal fissure, into the orbit, where they are 
distributed to the several muscles of the eye. The third supplies all 
the muscles except the external rectus, supplied by the sixth, and 
the superior oblique, supplied by the fourth. These nerves may 
either partially or completely lose their function, and produce corre- 
sponding paresis or paralysis of the dependent muscles. The nerves 
may be affected by lesions of their centers or of any part of their trunks. 
Tumors of the brain, lesions of the blood-vessels, ' meningitis, or 
peripheral neuritis, as in diphtheria, are most frequently encountered. 
The possibility of congenital strabismus or inequality of the pupils must 
always be borne in mind. 

Paralysis of one or more ocular muscles produces (1) an abnormal 
position of the globe of the eye or dilatation of the pupil from con- 
traction of the unopposed antagonists. (2) Impairment or loss of 
certain motions of the eye. (3) Diplopia. (4) Secondary deviation. 
If, with the sound eye covered, the patient fixes the affected eye upon 
an object before him, the sound eye will be found displaced in the 
direction of the action of the weak or paralyzed muscle. Thus, if the 
right internal rectus is affected, the left eye will, under these condi- 
tions, be found displaced outward. (5) Erroneous projection, and 
possibly vertigo. 

Paralysis of the third nerve results in ptosis, the eyeball is rotated 
outward and almost immovable, motion of the globe upward, downward 
or inward being particularly weak. Dilatation of the pupil may or may 
not be present. 

Paralysis of the fourth nerve alone causes but slight disturbance 
of motion. On looking downward the eye turns slightly inward and 
diplopia results. Thus on going downstairs the steps appear double. 

Paralysis of the sixth nerve produces internal strabismus, with 
inability to rotate the eye outward. Paresis of ocular nerves results 
in varying degrees of the disturbances caused by complete loss of 
function. 

Pupillary Irregularities. — Inequality of the pupils (anisocoria) of 
moderate degree is common in healthy persons. IMarked inequality 



TRIGEMINAL NERVE 



489 



usually indicates some definite lesion. It is most often associated with 
meningitis or cerebral hemorrhages, tabes, dementia paralytica, or tumor 
of the neck or upper part of the cord. 

The Argyll-Robertson pupil is indicated by a loss of the normal 
response to light with preservation of pupillary contraction in accom- 
modation. Alyosis is usually associated. The condition is closely asso- 
ciated with syphilis, and is most frequent in tabes dorsalis. 

Nystagmus, rhythmical oscillation of the eyes, usually from side 
to side, is met with in a variety of conditions. It is common in the 
blind or those with defective vision. It is most frequent in multiple 
sclerosis or lesions in the posterior fossa, especially those involving the 
cerebellum. 

The treatment of these conditions depends upon the cause. Per- 
sistent ocular palsies demand correction by prisms. 

TRIGEMINAL NERVE 
(Fifth Nerve) 

This nerve consists of both sensory and motor elements. The sen- 
sory portion supplies the orbit, the face, the scalp from the vertex to 
the ramus of the inferior maxilla and the mucous membranes of the 
nose and mouth. From the Gasserian ganglion these fibers pass to the 
pons, where they end in an extensive center. The motor fibers also find 
their center in the pons. Of the three branches the ophthalmic leaves 
the cranial cavity through the sphenoidal fissure, the superior maxillary 
through the foramen rotundum, the inferior maxillary (the motor por- 
tion) through the foramen ovale. 

This nerve may, therefore, be involved in lesions of the pons, by 
tumors or meningitis at the base of the brain, or fractures of the base 
(very rarely). The Gasserian ganglion is the probable seat of the 
lesions underlying herpes labialis and facial neuralgia. 

Paralysis of the fifth nerve shows itself by loss of sensation in the 
face and anterior portion of the scalp, by some impairment of smell 
due to dryness of the nasal fossae, and taste may be impaired over the 
anterior two-thirds of the tongue. The muscles of mastication are 
paralyzed, as can be appreciated, by placing the fingers just below the 
inferior maxillary articulation during the action of chewing. The lower 
jaw can be moved only to the sound side, and the mouth cannot be 
widely opened (digastric and mylohyoid paralysis). 

Trismus, tonic spasm of the muscles of the lower jaw, is a symptom 
of tetanus and sometimes of tetany. It may also occur in pontine 
lesions, as a reflex from carious teeth or periostitis of the jaw, or in 
hysteria. Clonic spasms, with rhythmic movements of the jaw, occur 
in meningitis, convulsions, epilepsy, hysteria and paralysis agitans. 
"Grinding the teeth" during sleep is a common occurrence in children, 
restless or disturbed for any reason. 



490 



DISEASES OF THE NERVOUS SYSTEM 



THE FACIAL NERVE 
(Seventh Nerve) 

The facial nerve nucleus, after the manner of the cerebral nerves, 
has a center in the floor of the fourth ventricle (pons Varolii), but it 
has also a definite cortical center in the loAver portion of the motor 
area ventral to the fissure of Rolando. Axones passing from cells in 
this area follow the motor tract to the pons, crossing just before reach- 
ing the nucleus. Emerging from the lateral aspect of the pons the 
nerve passes into the Fallopian canal, around the inner wall of the 
tjTupanum and emerges from the stylomastoid foramen. The nerve 
supplies the muscles of expression, the platj^sma, part of the digastric 
and stylohyoid muscles, and gives a small twig to the stapedius muscle 
of the ear. 

Paralysis of the facial (Bell's palsy) nerve may result from (1) 
lesions of the cortex or motor tract above the pons (supranuclear 
paralysis). (2) Lesions of the nucleus (nuclear paralysis). (3) 
Lesions of the nerve-trunk (infranuclear or peripheral paralysis). 

1. Supranuclear paralysis is regularly part of a hemiplegia, and 
may be caused by any of the lesions producing that condition, hemor- 
rhage, tumors, etc. The facial palsy is on the same side as the paralysis 
of arm and leg. It is distinguished from peripheral palsy by the pres- 
ervation of the electrical reactions, and the fact that, as a rule, the 
orbicularis palpebrarum, frontalis and corrugator muscles are spared. 

2. Nuclear paralysis, due to lesions in the pons, will regularly 
be accompanied by affections of the fifth, sixth or eighth nerves from 
involvement of the adjacent nuclei. Otherwise it does not differ from 
peripheral palsy. Crossed paralysis, paralysis of the seventh nerve 
on one side with loss of power in arm and leg of the other side, results 
from lesions in the lower half of the pons such that they involve the 
nucleus of the seventh nerve and the motor tract, the fibers of which 
have not yet crossed, the decussation occurring in the medulla. 

3. Peripher^u. paralysis. (1) The nerve may be involved in proc- 
esses at the base of the brain, meningitis, tumors, or fracture. 

(2) In the Fallopian aqueduct, inflammatory processes (otitis media, 
or caries of the bone) may involve the seventh nerve. The eighth 
nerve may suffer at the same time, with resulting deafness. 

(3) In the neck paralysis may result (a) from traimia of any kind 
or division during operations; (b) from syphilis, especially in the sec- 
ondary period; (c) from exposure to cold; (d) it may be associateil 
with herpes. 

Symptoms. — Facial paralysis is usually diagnosticated on sight. 
The affected side of the face appears flat, and the lips are drawn 
toward the sound side. If the paralysis involves all branches, the brow 
cannot be wrinkled, frowning is impossible, the eye is imperfectly 
closed, sniffing, whistling and speaking are impaired. In supranuclear 
paralysis, the upper branches often escape, and the forehead and eye 
may not be affected. 



THE AUDITORY NERVE 



491 



Certain points may closely localize the site of the affection. If 
the nerve is involved between the genu and the origin of the chorda 
t3^mpani, the sense of taste may be lost on the anterior two-thirds of 
the tongue. Lesions beyond that point have no such influence. 

If the lesion is located centrally to the origin of the nerve supply- 
ing the stapedius muscle, increased sensitiveness to low tones may be 
noted. In the supranuclear type the electrical reactions remain normal; 
in the nuclear or peripheral palsy the reaction of degeneration obtains. 

Course. — Facial palsy regularly recovers. In hemiplegia the re- 
covery may be only partial, but is usually rapid. Traumatic palsy may, 
however, be permanent. 

Treatment. — In most cases no treatment is required. The under- 
lying cause, such as syphilis or otitis media, should be appropriately 
treated. Electricity and massage may be employed as for other 
paralyses. 

Spasm. — Localized or general spasm of the facial muscles may occur. 
These usually belong in the category of habit spasms ordinarily affecting 
the muscles of the eye and adjacent parts of the face (blepharospasm). 
There is rapid, rhythmic action of the affected muscles. 

Treatment. — Any source of irritation, especially rhinitis or aden- 
oids, must be removed. The general condition of the patient must be 
considered and measures employed to correct nervousness. In severe 
cases division of the nerve may be required. 

THE AUDITORY NERVE 
(Eighth Nerve) 

The spinal centers of the eighth nerve are in the lower portion of 
the floor of the fourth ventricle. The nerve emerges from the medulla 
just below the pons Varolii, passes forward, enters the auditory canal, 
and at its bottom divides into two branches: the cochlear, concerned 
with hearing, and the vestibular, whose function is the maintenance of 
equilibrium. 

The cochlear branch is more frequently affected in its course than 
the vestibular. The cortical center for hearing is the superior tem- 
poral convolution. The cells of this center are connected by their axones 
with the spinal centers. Lesion of the center or of this tract produces 
the condition of word-deafness in which words are heard as sounds, 
but not understood. 

Either branch of the nerve may be involved in the degenerations 
•complicating cerebrospinal fever and diphtheria, the cochlear espe- 
cially, with resulting deafness. Tumors, hemorrhage, or fracture of the 
base of the cranium may involve the whole nerve. A primarj^ degen- 
eration sometimes occurs in locomotor ataxia. 

Hyperesthesia of the eighth nerve, or hyperacusis, is common 
in headache, in hysteria, or neurasthenia. It rnrf^ly results from cere- 
bral disease. Tinnitus aurium includes various snl)jectiv(' sciisalions 
of ringing, roaring, ticking or buzzing noises in the ear. The disorder 



492 



DISEASES OF THE NERVOUS SYSTEM 



most frequently results from neurasthenia, but may be caused by the 
pressure of wax or by definite disease of the middle or internal ear. 

Deafness may result from various causes. It is important to test 
the integrity of the nerve. This may be done by employing a tuning 
fork or watch, comparing the hearing under normal conditions with 
that obtained by closing the external meatus and holding the fork or 
watch against the mastoid process. If the cochlear nerve itself is diseased, 
the sound is not heard under the latter circumstances. Under normal 
conditions the sound is readily transmitted through the bone to the 
cochlea. If bone transmission is better than air there is then some 
obstruction or disease of the middle ear. 

The vestibular nerve is rarely affected. Disease of the vestibular 
portion gives rise to vertigo, nystagmus and loss of co-ordination of the 
muscles of the head, neck and eyes. 

Vertigo is dependent upon some disturbance of the complex mus- 
cular adjustments by which equilibrium is maintained in various posi- 
tions. There are many causes of vertigo. It is a common symptom 
of neurasthenia and hysteria, of muscular and other eye defects, of 
disease of the internal or middle ear, of tumors of the brain (especially 
those involving the cerebellum), and other cerebral lesions, such as 
arteriosclerosis. It may result from cardiac disease or gastro-intestinal 
disorders, particularly autointoxication. 

Meniere ^s Disease. — An affection described by a French physician, 
characterized by attacks of vertigo and tinnitus, associated with vomit- 
ing and sometimes loss of consciousness. The paroxysms occur irregu- 
larly, sometimes several in a day, sometimes at long intervals. The 
affection has been attributed to disease of the labyrinth, but the pa- 
thology is unsettled. The more carefully vertigo is studied the more 
frequently definite cause is found, and the diagnosis of Meniere's dis- 
ease is now rarely heard. 

Treatment. — Careful examination for local disease of the ear and 
appropriate treatment of any lesion there present are essential in both 
tinnitus and vertigo. If further examination shows other definite con- 
ditions, such as neurasthenia, arteriosclerosis, disease of the heart which 
may be causative, treatment must be planned accordingly. 

For Meniere's disease various remedies are recommended, such as 
bromide or iodide of potassium; the salicylates and quinine have been 
employed with doubtful efficacy. 

THE GLOSSO-PHARYNGEAL NERVE 
(Ninth Nerve) 

The center for the ninth nerve lies beneath the fovea in the floor 
of the fourth ventricle. It leaves the cranium by the jugular foramen, 
and supplies motor and sensory branches to the pharynx and adjacent 
parts. Its most disputed function lies in supplying the sense of taste 
to the posterior one-third of the tongue. 



THE PNEUMOGASTRIC NERVE 



493 



Symptoms. — The pharyngeal symptoms of bulbar paralysis are 
explained by lesion of the ninth nerve. The nerve may be affected 
by tumors or meningitis, causing difficulty in swallowing. 

Disturbances of taste on the posterior part of the tongue result from 
lesions of the ninth nerve. These are tested for by tiie application of 
solutions of quinine (bitter), saccharin (sweet), vinegar (acid) on the 
protruded tongue. The tongue must be held out till decision is given. 
A feeble galvanic current giving rise to a metallic taste may be em- 
ployed. Salivary secretion may be affected by disease of this nerve. 

THE PNEUMOGASTRIC NERVE 
(Tenth Nerve) 

The center of the vagus lies in the floor of the fourth ventricle, 
so closely related to that of the ninth as to be with difficulty distin- 
guishable from it. The nerve leaves the cranium through the jugular 
foramen, and has the widest distribution of any of the cranial nerves. 
It contains both motor and sensory fibers, giving motor supply to some 
of the phar^^ngeal muscles, to the larynx, trachea and bronchi, and to 
the whole gastro-intestinal tract excepting the rectum, and sensation 
to the same general territory, and also the dura, ear and pericardium. 
The cardiac nerves also form part of the vagus. 

Symptoms. — The nerve may be involved at its center, especially in 
the glosso-labio-laryngeal paralysis, in diphtheria, anterior poliomyelitis 
and the like. At the base of the brain it may be compressed by tumors, 
or involved in meningitis. 

In the neck it is subject to traumatism, blows or gunshot wounds, 
the pressure of tumors or section in the course of operations, or it may 
be affected by neuritis. 

The symptoms will depend upon the particular branches affected. 

Pharyngeal Branches. — Paralysis follows diphtheria, meningitis, 
tumors, bulbar palsy and the like. Difficulty in swallowing results. 
Food may pass into the larynx or be regurgitated through the nose. 
Spasm of the pharynx occurs in hysteria (globus hystericus) and other 
nervous affections, especially hydrophobia. 

Laryngeal Branches. — Paralysis of the larynx. Several types of 
laryngeal paralysis are recognized. 

In general hoarseness, aphonia, cough, stridulous respiration or 
dyspnea may be caused by laryngeal paralysis. 

Laryngoscopic examination is necessary to determine which muscles 
are affected. 

Bilateral Abductor Paralysis. — The cords are approximated and can- 
not be abducted. Stridulous respiration and severe dyspnea result, 
w^hile phonation is preserved. The condition develops from involve- 
ment of the center in bulbar palsy, or tabes. It may be caused by 
pressure on both vagi, or by exposure to cold. Some cases are hysterical. 

Unilateral Abductor Paralysis. — This results from pressure on one 



494 



DISEASES OF THE NERVOUS SYSTEM 



nerve, especially upon the recurrent laryngeal by aneurisms. The left 
nerve is most frequently involved. The cord on the affected side does 
not move in respiration or phonation. 

Adductor Paralysis. — The cords cannot be approximated and phona- 
tion is impaired or lost. Hysteria is the usual cause. 

Spasm of the larynx occurs in laryngismus stridulus, and is un- 
doubtedly present in most cases of acute laryngitis (croup), diphtheritic 
or not, in children. For this reason the relaxation produced by nausea 
and vomiting gives at least temporary relief in such conditions. 
Paroxysmal attacks of laryngeal spasm explain the laryngeal crises of 
tabes. 

Anesthesia of the larynx occurs in bulbar palsy and in diphtheritic 
neuritis. Dysphagia is also present. Food may enter the respiratory 
passages and bronchopneumonia result. The condition may be hysterical. 

Cardiac Branches. — Motor. Vagus stimulation may cause slowing 
of the heart action, or paralysis may result in great rapidity, but neither 
of these conditions is ordinarily realized unless both nerves are involved. 
For this reason disturbances of the heart definitely traceable to vagus 
injuries are rare, except as part of a diphtheritic or other general 
neuritis. 

Sensory cardiac disturbances are treated under Neuroses of the 
Heart." 

Pulmonary Branches. — Bronchial asthma may be due to spasm 
of the bronchial muscles produced by vagus irritation. Slowing or 
quickening of respiration may result from disease of these branches, 
but again only in case of involvement of both vagi. 

Esophageal and Gastric Branches. — Spasm of the esophagus is 
attributable to vagus irritation. The various neuroses of the stomach 
are evidences of disturbance of vagus function. The gastric crises of 
tabes are doubtless due to central lesions. 

THE SPINAL ACCESSORY NERVE 
(Eleventh Nerve) 

The smaller part of this nerve joins the vagus, and is considered as 
part of it. The spinal portion supplies the sternomastoid and trapezius 
muscles, and is purely motor. The center for the spinal accessor}^ is 
very extensive, extending from the medulla to the fifth or sixth cervi- 
cal segment. The nerve passes through the jugular foramen, pierces 
the sterno-mastoid in the neck, and crosses the occipital triangle to end 
in the trapezius. 

Paralysis of one spinal accessory nerve is shown by disability in 
rotating the head to the other side (sterno-mastoid), by drooping of the 
shoulder, inward rotation of the angle of the scapula, and disability in 
raising the arms (trapezius). Bilateral palsy results in loss of power 
to lift the head (sterno-mastoid) or to prevent it falling forward 
(trapezius). 



HYPOGLOSSAL NEEVE 



495 



Paralysis results from disease of the spinal cord, progressive mus- 
cular atrophy (bilateral palsy), cervical myelitis, syringomyelia and 
pachymeningitis, or caries of cervical vertebrge (tuberculosis). In 
the latter cases the lesion is usually one-sided. 

Torticollis or Wry-neck. — The abnormal position of the head and 
face caused by unequal action of the cervical muscles is in large part 
due to the action of stemo-mastoid and trapezius, though other muscles 
of the neck are involved. 

Congenital cases are due to lack of development or injuries of 
the sterno-mastoid at birth. Facial asymmetry is usually present. It 
is commonly not noted at birth, and may not be for several years. It 
is regularly relieved by tenotomy. 

Acquired torticollis or temporary wry-neck may be one form of 
muscular rheumatism or may be caused by adenitis, the nodes under- 
lying the sterno-mastoid being tender and causing spasm of the mus- 
cle, or by caries of cervical vertebra. 

Spasmodic wry-neck occurs from unknown causes and the lesions 
are unknown. The condition is chronic. The head is drawn down- 
ward and toward the affected side, the chin and face upward and 
toward the opposite side. Other muscles than those supplied by the 
spinal accessory are involved. The condition is usually a tonic spasm 
of the affected muscles, but clonic movements are seen in some cases, 
and in rare instances the clonic spasms are the more important feature. 

Treatment. — The temporary form is to be treated according to the 
cause, as rheumatic or gouty, or due to adenitis or caries. In acute 
cases rest is most important. This may be secured merely by lying with 
the head in a soft pillow, or by sand bags placed at the sides of it. Heat 
and gentle friction are grateful. Aspirin or salicylates may be given, as 
for muscular rheumatism. 

If adenitis or caries of the vertebrae is present, treatment must be 
planned accordingly. For the spasmodic form, the only effective treat- 
ment is orthopedic or operative. 

HYPOGLOSSAL NERVE 
(Twelfth Nerve) 

The cortical center is the lower part of the anterior central gyrus. 

The spinal center is in the floor of the lower portion of the fourth 
ventricle and the adjacent part of the medulla. The nerve leaves the 
spinal canal by the anterior condyloid foramen, lies deeply in the neck, 
and passes forward near the angle of the jaw to supply the muscles 
of the tongue, its function being purely motor. 

Lesions of the cortical center are part of a hemiplegia. Unilateral 
paralysis without atrophy or reaction of degeneration results. 

Nuclear lesions are most common in bulbar paralysis and pro- 
gressive muscular atrophy. The nerve may be involved by tumors or 
basal meningitis, by trauma or lead poisoning. The lesions may affect 
one or both nerves. 



496 



DISEASES OF THE NERVOUS SYSTEM 



In one-sided paralysis of the hypoglossal the tongue when pro- 
truded deviates toward the affected side. Atrophy occurs in the periph- 
eral or nuclear lesions. • 

In bilateral paralysis the tongue cannot be protruded, Is atrophied, 
and there are difficulties in swallowing and speech. Fibrillary tremors 
may also be seen. 

Spasm of the glossal muscles is rare. It may occur as part of chorea, 
hysteria, epilepsy or other convulsive disorder; it may be either uni- 
lateral or bilateral. A clonic form marked by rapid, rhythmic pro- 
trusion of the tongue has been observed. Recovery is the rule in all 
cases. 

DISEASES OF THE SPINAL NERVES 

CERVICAL PLEXUS 

Neuralgia may affect the nerves of this region, causing pain in the 
nape of the neck and the occiput. Neurasthenia is the most frequent 
cause, but caries of the spine, arthritis deformans, tumors and aneu- 
risms of the vertebral artery must be excluded. Tender points midway 
between the mastoid and the first cervical vertebra may be present. 
Organic lesions having been excluded, treatment must be that of neu- 
ralgia. 

Phrenic Nerve. — Paralysis of one or both phrenic nerves may 
occur. Paralysis of the phrenic nerve may result from involvement of 
the anterior horns at the level of the third or fourth cervical nerves, 
from anterior poliomyelitis or ascending paralysis or multiple neuritis, 
such as follow^s diphtheria or lead poisoning. In rarer cases it fol- 
lows vertebral caries or pachymeningitis. 

Unilateral paralysis gives but few symptoms, and is often over- 
looked. Bilateral paralysis shows itself by immobility of the diaphragm. 
Respiration is thoracic, and the liver and spleen are no longer pushed 
down by inspiration. The epigastrium is depressed in inspiration and 
rises in expiration. Dyspnea and cyanosis develop in some cases. 
Coughing is difficult and mucus collects in the bronchi. 

The Diagnosis. — Immobility of the diaphragm from other causes, 
diaphragmatic pleurisy, emphysema, large pleural effusions must be 
excluded. Many women use the diaphragm poorly under normal con- 
ditions. The development of signs of phrenic paralysis in the course 
of anterior poliomyelitis, or ascending paralysis, or multiple neuritis is 
important. Treatment is that of the underlying condition. Thoracic 
respiration should be favored. In severe cases the head should be low- 
ered or the feet raised to favor the expulsion of mucus from the bronchi. 

Hiccough. — This is caused by an associated sudden contraction of 
the diaphragm and closure of the glottis, often repeated rhythmically. 

The exciting causes are varied, and may be grouped thus: (a) Irri- 
tative, the spasm being excited by some irritation in the territory of 
the pneumogastric, such as too hot food, local disease of the esophagus 



DISEASES OF THE SPINAL NERVES 



497 



near the diaphragm, gastric or intestinal indigestion, any abdominal 
inflammation, especially gastritis or peritonitis, (b) Constitntional, 
arising from gout, diabetes or chronic nephritis, (c) Neurotic, in such 
conditions as hysteria, epilepsy and brain tumors. 

Treatment. — Holding the breath as long as possible will stop mild 
attacks. AYashing out the stomach, an ether spray on the abdomen, 
the hypodermic use of apomorphine, morphine, or pilocarpine, inhala- 
tions of ether, chloroform, or amyl nitrite, galvanization of the phrenic 
nerve, and pressure upon the nerve between the heads of the sterno- 
mastoid, all have been tried. 

THE BRACHIAL PLEXUS 

Tumors, enlarged glands or aneurisms may afPect the brachial plexus 
by pressure. Inflammation is very rare, but may follow an ascending 
neuritis. Trauma in one or another form is the common cause of par- 
tial or complete paralysis. Dislocations of the humerus, especially the 
subcoracoid, blows on the shoulder, improper crutches, traction in the 
axilla during delivery, the pressure of a cervical rib, have all caused such 
disturbances. Loss of power in the arm, partial or complete, is the chief 
symptom. Sensory symptoms, such as tingling or numbness, may occur. 
The entire plexus or one of its branches may be involved, the distribu- 
tion of paralysis and anesthesia varying accordingly. The result of the 
involvement of the more important nerves may be summarized as follow^s : 

(a) The Long Thoracic. The serratus magnus is paralyzed, and in 
consequence the angle and posterior border of the scapula stand out 
from the chest "like wings," especially when the arms are extended 
forward. The paralysis is usually associated with that of other muscles 
of the shoulder girdle. 

(b) Circumflex Nerve. The deltoid and teres minor are paralyzed. 
Wasting is marked ; the arm cannot be raised ; sensation is commonly 
impaired. 

(c) Musculo-spiral Nerve. This nerve is especially easily injured, 
as it winds around the upper arm, so that paralysis has resulted from 
sleeping with the arm over the back of a chair or lying on the 
arm, or allowing the arm to rest on the edge of the table during opera- 
tions. Lead or alcoholic poisoning is a frequent cause. Wrist-drop 
and inability to extend the first phalanges are characteristic. Sensory 
disturbances are rarely marked. The reaction of degeneration develops 
in severe cases. 

(d) Ulnar Nerve. Paralysis may result from neuritis or trauma. 
The first phalanges cannot be flexed, the others cannot be extended, and 
claw-hand or "main en griffe" results. The hand is drawn to the 
radial side and adduction of the thumb is impossible. Sensation may be 
lost on the backs of two and a half fingers on the ulnar side, and on 
the palmar surface of one and a half. 

(e) Median Nerve. Paralysis results from trauma or neuritis, and 
32 



498 



DISEASES OF THE NERVOUS SYSTEM 



rarely is the median alone involved. The forearm cannot be pronated 
more than half way. The wrist flexes toward the ulnar side. The 
second phalanges of all the fingers and the terminal ones of the index 
and middle cannot be flexed. The proximal phalanges can be flexed 
through the interossei. The thumb cannot be flexed or opposed. The 
wrist can be flexed only w^hen adducted. Sensation is lost or impaired 
both front and back, except over the little and the inner half of the 
ring finger. Atrophy is marked. 

The prognosis depends upon the cause and the severity of the lesion. 
Recovery is the rule. 

LUMBAR PLEXUS 

Branches of this plexus may be affected by the pressure of tumors, 
lymph-nodes or psoas abscess, or by caries of the vertebras. The obtura- 
tor nerve may be injured in parturition and paralysis of the addu3tors, 
shown by inability to cross one leg over the other, result. The anterior 
crural may be impaired by wounds or dislocation of the hip joint. 
Paralysis of the extensors of the knee with wasting and anesthesia on 
the inner aspect of the thigh and leg results. The external cutaneous 
nerve may be affected by neuritis. Tenderness of the nerve as it passes 
under Poupart's ligament just internal to the anterior superior spine 
is found, and there are pain and paresthesia in the territory of the 
nerve, lasting indefinitely. Division of the nerve has been resorted to. 

SACRAL PLEXUS 

The branches of this plexus may be injured by pelvic tumors or 
inflammations, or during parturition. Neuritis may follow sciatica. 

The great sciatic nerve. The flexors of the leg and^all the muscles 
below the knee are paralyzed, and there is anesthesia of the outer half 
of the leg and both sole and dorsum of the foot. 

The external popliteal nerve. Paralysis is common in peripheral 
neuritis. The peronei, the tibialis anticus and both extensors of the 
toes are paralyzed. Drop-foot and steppage gait result. Sensation is 
lost on the outer half of the front of the leg and the dorsum of the 
foot. 

Internal popliteal nerve. Paralysis is rare. The foot and toes 
cannot be extended. The patient cannot stand on tip-toe. In severe 
and old cases talipes calcaneus results. 

S€IATICA 

A neuritis or neuralgia of the great sciatic nerve. Adult and vigor- 
ous men and women suffer from the affection. Exposure to cold, over- 
exertion, gout and rheumatism are regarded as causative factors. 
Pressure of spinal or pelvic tumors, especially those of the uterus or 
ovaries, new growths, impacted feces and the like may cause sciatica. 
In many cases no satisfactory cause is to be found. Anatomically both 



DISEASES OF THE SPINAL NERVES 



499 



a perineuritis and interstitial neuritis have been found in the few cases 
examined. 

Symptoms. — Pain in the course of the nerve, mild or severe, con- 
stant or intermittent, is present. Beginning at the upper part of the 
nerve the pain extends till it affects the whole territory. Sensitive 
points over the course of the nerve are present. Walking increases the 
pain, and seeking relief the patient walks on the toes. In severe cases 
the patients are bed-ridden. 

AVasting and cramps occur in prolonged cases. Flexion of the 
thigh with the leg straight increases the pain. 

Duration and course are both variable. Sciatica may last weeks, 
months, or even years. Relapses are common. 

In many cases the affection seems to gradually lessen with little re- 
gard to treatment. 

Diagnosis. — Disease of the spine must be carefully sought for. 
Pelvic tumors must be excluded by examination of the abdomen, and 
rectum or vagina. Hip-joint disease must be excluded by freedom of 
motion in the joint, so long as the thigh is not flexed. Attempt to 
flex the thigh with the leg straight increases the tension on the sciatic 
nerve and elicits pain in sciatica. Sacro-iliac disease must be ex- 
cluded by the harmlessness of pressure on the sides of the pelvis and 
the absence of local signs. 

Tender points along the course of the sciatic nerve help to confirm 
the diagnosis. 

Treatment. — Rest is the prime factor. Careful dieting, sunshine 
and fresh air are important, A long splint may be employed. Hot 
water, poultices of flaxseed or mustard, blisters, afford temporary 
relief. The thermo-cautery has been much used, but the continuous 
heat of poultices is more successful. Phenacetin or antifebrin give 
only temporary relief, and their continued use is depressing. Cocaine 
or morphine hypodermatically may be employed as last resorts, but 
the danger of habit is great. 

Injections of distilled water, alcohol or even choloroform into the 
nerve have been practiced. 

The galvanic current has sometimes given relief. Nerve stretching 
by cutting down on the nerve and making sufficient traction upon it to 
lift the leg has been successful. 

In the chronic cases attention to feeding and the beneficent in- 
fluences of fresh air and sunshine are more important than local meas- 
ures. In the very thin forced feeding is of value. 

DISEASES OF THE SPINAL CORD AND MENINGES 

SPINAL PACHYMENINGITIS 
Definition. — An inflammation of the dura of the cord, on either its 
external or internal surface. 

Etiology. — External pachymeningitis occurs in conjunction with 



500 



DISEASES OF THE NERVOUS SYSTEM 



spinal injuries and tumors or inflammations (tuberculosis especially) 
of the vertebrae. It may be acute or chronic, depending on the activity 
of the bone disease. 

Internal pachymeningitis occurs as part of the external processes, 
but there is also an independent form, analogous to the hemorrhagic 
pachymeningitis of the brain, which occurs especially in syphilitic, 
alcoholic or insane subjects. 

Morbid Anatomy. — The dura is much thickened and an exudate 
is found on its external or internal surface or both. The exudate is 
usually purulent or hemorrhagic. In tubercular cases it may be cheesy. 
In the hemorrhagic form the internal surface is coated with a delicate 
vascular membrane, and there are punctate or larger hemorrhages. 
Blood cysts are sometimes found in old cases. 

Symptoms. — These include: (1) Pain, hyperesthesia or anesthesia 
in the area of the nerves whose roots are pressed upon. The pain may 
be very severe. (2) Spasm, weakness or paralj^sis and atrophy in 
affected muscles. The arms are most often involved and typical "main 
en griff e" may be produced. (3) Secondary degeneration of the cord 
may follow, with involvement of the legs, ending in a spastic paraplegia. 

Diagnosis. — An X-ray examination of the spine should be made to 
exclude tubercular disease or tumors. The Wassermann reaction and a 
spinal lymphocytosis should be present in syphilis. 

From amyotrophic lateral sclerosis the disease is distinguished by 
the marked sensory disturbances. From syringomyelia by the preser- 
vation of temperature sense. Tumors are excluded with difficulty, as 
the symptoms are identical. 

Prognosis. — The disease is chronic — lasting several years — and is 
usually fatal from intercurrent infections, especially of the bladder 
and urinary tract, or from exhaustion. 

Treatment. — If syphilis is present, a thorough anti-syphilitic treat- 
ment is indicated. (See page 450.) Otherwise counter-irritation by 
blister or the actual cautery, rest and symptomatic treatment must be 
relied on. 

SPINAL LEPTOMENINGITIS 
Definition. — An acute or chronic inflammation of the pia mater of 
the cord. 

ACUTE SPINAL LEPTOMENINGITIS 

Etiology. — The pia mater of the cord being continuous with that of 
the brain is regularly involved with it. Acute spinal leptomeningitis 
is therefore usually part of a cerebral meningitis, and is dependent 
on the same causes. (See page 524.) An acute suppurative inflamma- 
tion of the spinal meninges may occur independently in the terminal 
stages of some chronic diseases, such as chronic nephritis, or from the 
invasion of suppurative processes involvino- the spinal vertebra\ 

Morbid Anatomy. — The lesions are those of the corresponding cere- 
bral process. 



AFFECTIONS OF THE BLOOD-VESSELS 



501 



Symptoms. — These are part of the general picture of cerebrospinal 
meningitis. Rigidity of the neck, spasm or paralysis of muscles of the 
trunk or extremities, the sensory and vasomotor disturbances of these 
parts may be explained by involvement either of cerebral or spinal 
centers. In the independent cases, sensory and motor disturbances 
arise in the parts supplied by the affected segments of the cord. Pain 
and spasm or loss of power are most prominent. 

Treatment is that of cerebrospinal meningitis. 

CHRONIC SPINAL LEPTOMENINGITIS 

Etiology. — Chronic inflammation of the spinal pia mater rarely 
results from the acute form, but follows syphilitic or tubercular lesions 
of the vertebrae or cord, or results from injury. 

Morbid Anatomy. — The pia mater of the cord is thickened, opac[ue, 
adherent. Gummata or tubercles may be present. The vertebrge or 
cord show corresponding lesions. 

Symptoms.^ — Pain, spasm or paralysis in the parts supplied by the 
affected segments of the cord results. Some of the symptoms produced 
by tubercular or specific disease of the cord or vertebrie are explainable 
in this manner, but the symptoms due to the lesion of the membranes 
are usually obscured by the more important affection of the bones or 
cord, and the diagnosis is that of the primary condition. 

Treatment. — The underlying condition (syphilis or tuberculosis) 
must be treated. Counter-irritation, local applications of heat or cold, 
and spinal douches may be employed. 

AFFECTIONS OF THE BLOOD-VESSELS AND CIRCULATION 

OF THE CORD 

Hyperemia. — Congestion occurs as part of acute inflammation of the 
membranes or of acute myelitis, poliomyelitis and the like. It need not 
be considered separately. 

Anemia. — In some cases of severe anemia, especially pernicious 
anemia, marked changes in the spinal cord are found. The symptoms 
of these spinal changes may precede or overshadow those of the anemia. 
The symptoms vary. They are usually limited to the lower extremi- 
ties and are of several types. (1) Pain and paresthesia (numbness, 
tingling, etc.) are commonly present, either in feet or hands. 

(2) Spastic. The patellar reflexes are increased, the muscles and 
gait are spastic, weakness or paralysis are marked. 

(3) Ataxic. The reflexes are lost, the gait ataxic, and the picture is 
that of tabes dorsalis. 

Embolism and Thrombosis. — These lesions may occur under the 
conditions which cause cerebral embolism or thrombosis. They are not 
commonly recognized. 

Arteriosclerosis of spinal vessels occurs as part of the general- 



502 DISEASES OF THE NERVOUS SYSTEM 



ized process. Of recent years the resulting disturbances of function 
have received much attention under the designation of intermittent 
claudication or limp. (Erb.) (See page 232.) 

Hemorrhage into the cord (hematomyelia) . Bleeding into the sub- 
stance of the cord results most often from trauma, falls on the back or 
blows on the spine and the like. 

Exposure to cold, over-exertion and excessive coitus are also possi- 
ble causes. Such affections of the cord as myelitis, syringomyelia or 
tumors may be complicated by hemorrhage. 

Morbid Anatomy. — The hemorrhage may be large or small. Soften- 
ing and destruction of the cord vary with the extent of the hemorrhage. 
Not infrequently multiple foci are found. In old cases the blood is 
absorbed and only pigmented areas found. 

Symptoms. — Sudden onset of pain followed by paralysis, and then 
loss of sensation affecting the lower extremities or the whole body up 
to the neck, are characteristic. Rapid improvement in the symptoms, 
caused by resorption, is also suggestive. Incontinence of urine and 
marked constipation are usually present. Bed sores and cystitis are 
frequent complications. 

Gradual improvement usually follows and complete recovery is possi- 
ble. The presence of faradic response in a muscle or muscles is hope- 
ful, loss of it a sign of permanent paralysis. Death may result at once 
from extensive hemorrhages or in other cases follow sepsis from bed 
sores or cystitis. 

Treatment. — Protracted rest with care of the bowels and bladder 
is essential. Asepsis must be observed in catherization. After six or 
eight weeks, electricity, massage, passive and then active movements are 
employed to restore muscular power. 

CAISSON DISEASE 

Definition. — A condition characterized by pain and paralysis, usually 
paraplegia, met with in caisson or tunnel-workers on too rapid exit 
from the high-pressure chambers. 

Etiology. — In deep tunnels and caissons an artificial air pressure 
of several atmospheres is maintained to prevent the entrance of Avater. 
Under such pressure the blood becomes surcharged with gases. On the 
withdrawal of the pressure some part of these gases (0 and COo) must 
be rapidly discharged. Under normal conditions such discharge occurs 
in the lungs. If the fall of pressure is suddenly induced, these gases 
may be liberated internally, especially in the closed spinal canal, with 
resulting damage to the cord. Venous stasis similarly caused may play 
a part in the process. 

Indulgence in alcohol, heart or kidney disease, or illness of any kind 
predisposes to this affection. 

Prevention. — Examination of all tunnel workmen to exclude the 
unfit, shortening of the hours of work under high pressure to four or 
even to three hour "shifts," and installing exit chambers in which the 



AFFECTIONS OF THE BLOOD-VESSELS 



503 



men are required to remain from fifteen to thirty minutes, while the 
pressure is gradually lowered, have greatly reduced the number of 
eases. 

Lesions. — In recent cases congestion of the brain and spinal cord 
sometimes accompanied by minute lacerations is found; in long-stand- 
ing cases areas of softening in the cord and the appearances of a myelitis. 

Symptoms. — These may develop immediately on leaving the lock or 
only after three or four hours. Pains in the legs or abdomen, giving 
rise to the popular name of ' ' the bends, ' ' usually mark the onset. Loss 
of power may or may not follow. In severe cases paraplegia with com- 
plete loss of power and sensation in the lower extremities results. Sud- 
den death may occur. Headache, nausea, vomiting, tinnitus or deaf- 
ness, and retention of urine may accompany the onset. The milder 
symptoms disappear quickly; the severer cases run the course of a 
severe myelitis. Death may result from bed sores or cystitis, or recov- 
ery with weakness or partial loss of power in the legs may be the 
outcome. 

Treatment.— Return to the high pressure immediately may bring 
prompt relief from symptoms. Cabinets for this purpose are now pro- 
vided. Otherwise the treatment is that of myelitis. 

MYELITIS 
(Transverse or General Myelitis) 

Definition. — A localized degeneration or inflammation of the spinal 
cord involving the entire area of one or more segments. 

Etiology. — The term myelitis covers a number of affections of the 
spinal cord, agreeing only in the fact that they affect the total area 
of some part of the cord. The etiology is therefore diverse. Trans- 
verse myelitis may follow: (1) Certain acute infectious diseases, espe- 
cially the exanthemata, rheumatism, or septicemia. (2) The toxemia 
of pregnancy or the puerperium. (3) Syphilis in 75% of cases. 
Trauma, exposure to cold, and excessive sexual indulgence are regarded 
as contributory causes. 

Morbid Anatomy. — Softening of some part of the cord is found, 
and it may be diffluent or even purulent. Hyperemia or small hemor- 
rhages are found on the surface of the affected portion. On section 
the outlines of the gray and white substance are indistinct and the 
clear color and markings of the normal cord are lost. 

Microscopically the appearances include hemorrhages, infiltration 
about the blood-vessels, and degeneration of the ganglion cells. The 
degenerations may be traced upward or downward in the several tracts 
of the cord. In old cases the cord becomes sclerotic, and the ascend- 
ing and descending degenerations can be traced for some distance from 
the seat of softening. 

Bacteriology. — Staphylococci, streptococci and pneumococci have been 
found in various cases. No one organism is constant. 



504 



DISEASES OP THE NERVOUS SYSTEM 



Symptoms. — The onset may be sudden and acute with fever, or in 
children convulsions; or it may be gradual and insidious. Premonitory 
tingling, numbness, formication, hyperesthesia or girdle sensation may 
be felt. 

The extent and distribution of symptoms will depend upon the level 
of the cord affected. If the lesion is in the sacral portion only the lower 
extremities will suffer. If in the dorsal region part of the trunk also 
will be involved, and if the lesion be cervical all the trunk and the 
arms, as well as the legs, participate in the disturbance. The motor 
symptoms are most impressive. Power is lost in part or altogether. 

The legs, or both legs and arms, are partially or totally paralyzed. 
If the lesion is high, the diaphragm and respiratory muscles may be in- 
volved and dyspnea result. There is regularly difficulty in emptying 
the bladder and rectum, and retention and constipation, or incontinence 
from overflow result. 

Sensory symptoms are less pronounced. Sensation is lost in part 
or altogether. At the level of the lesion there may be a narrow zone 
of hyperesthesia. 

The deep reflexes are lost if the lesion involves the centers con- 
cerned in their production ; they are increased if the lesion is above these 
centers. Ankle clonus and exaggerated patellar reflexes are therefore 
common. Babinski's sign is present. 

Atrophy of the muscles occurs from disuse, and they become soft 
and flabby, but the electrical reactions are preserved. Rigidity may 
develop. Bed sores and cystitis are frequent and dangerous complica- 
tions. 

The duration of the affection varies from days to years. The con- 
dition tends to become chronic — the paralysis permanent with result- 
ing contractures and deformities, the incontinence established, bed sores 
or other septic infection (cystitis) troublesome. The patients die of 
exhaustion or from intercurrent infection. 

The course in some cases is swiftly fatal, in others life is prolonged 
for years. Recovery may occur in milder cases. 

Diagnosis. — The combination of paraplegia with loss of sensation 
and loss of control of the sphincters is characteristic. Compression of 
the cord by tumors or fracture or dislocations of the vertebra? must be 
excluded. 

Disseminated sclerosis must be excluded by the definiteness of the 
upper limit of the palsy and the absence of pupillary phenomena. 

Functional paralysis (hysteria) must be considered, especially in 
young women. Loss of control of the sphincters, the presence of Bab- 
inski's sign, as well as absence of other signs of hysteria, must be con- 
clusive. 

Syphilis must be sought for in other parts. A Wassermann reaction 
is important. The cerebrospinal fluid should be obtained by lumbar 
puncture and examined for organism.s and cells. A lymphocytosis 
favors the diagnosis of syphilis. 



COMPRESSION OF THE SPINAL CORD 



505 



Treatment. — In early syphilitic cases specific treatment should be 
pushed, salvarsan followed by both mercury and the iodides. 

In all cases, rest in bed, a reasonable diet and care of the bladder 
and rectum are essential. The catheter must be employed, if necessary, 
but under strict aseptic precautions. The bowels should be moved by 
laxatives or enemata. Careful nursing is essential to prevent bed sores. 

After some Aveeks (six or eight) massage, electricity and passive 
motion may be employed for the paralyzed parts, and the patient should 
be encouraged to try movements for himself. 

COMPRESSION OF THE SPINAL CORD 

(Compression Myelitis) 

Definition. — Interference with the functions of the spinal cord due 
to pressure. 

Etiology. — The most frequent cause is caries of the spine, due to 
tuberculosis. The resultant "knuckling" of the spine and possibly the 
products of inflammation serve to compress the cord, and more or less 
completely abolish its functions. Children suffering from Pott's disease 
therefore often present symptoms of compression. 

Aneurisms or other thoracic or abdominal tumors may erode the 
spine and compress the cord. 

New groivths of the spine itself or the membranes of the cord, 
abscesses, hemorrhages or gummata located within the spinal column, 
extreme lateral curvature, fracture or dislocation of the spine may have 
this result. 

Morbid Anatomy. — The cause of compression is found in caries of 
the spine or some of the other causes mentioned. The cord itself is 
smaller than normal and softened at the affected part. The outlines of 
gray and white matter may be obliterated, and the substances of the 
cord may be fluidified or in late cases replaced by fibrous tissue. 

Microscopically the cells of the cord are degenerate or absent, and 
above and below respectively in long-standing cases there will be de- 
generation of the ascending or descending tracts of the cord. 

The SYMPTOMS, like those of a myelitis, depend upon the level of 
the cord affected. In the great majority of cases the compression is in 
the dorsal or lumbar region. Weakness of the legs, increasing grad- 
ually to complete loss of power, loss of control of bladder and rectum, 
and loss of sensation in the lower extremities usually develop. In cases 
of fracture or dislocation these symptoms come on suddenly. If the 
lesion is cervical, loss of power and sensation is seen in the arms, and 
there may be dyspnea and cyanosis. 

At the upper margin of the area of anesthesia there may be a narrow 
band of hyperesthesia. 

The reflexes, if their centers are involved, are lost: if the lesion is 
above these centers, they are exaggerated. Babinski's reflex should 
be present. 



506 DISEASES OF THE NERVOUS SYSTEM 



The course of the affection depends upon the cause. Cases due to 
Pott's disease may, under treatment, become quiescent or recover. If 
due to giunmata, recovery follo^^^ specific treatment. In other cases 
the condition grows gradually worse, and the patient dies of exhaustion, 
bed sores, cystitis or pyelonephritis. 

Treatment. — The cause must be treated. Pott's disease requires 
proper apparatus, and the measures applicable to tuberculosis in gen- 
eral. Rest in bed upon the back and extension are sometimes required. 

Gummata demand the trial of salvarsan. followed by iodide of potas- 
sium in increasing doses, and mercurials. Otherwise the treatment must 
be wholly symptomatic. The danger of bed sores and cystitis should be 
remembered. 

ACUTE POLIOMYELITIS 
(Acute Anterior Poliomyelitis or Infantile Spinal Paralysis) 

Definition. — An acute infectious disease characterized by acute in- 
flammation and degeneration of the gray matter of the spinal cord, 
especially the anterior horns, and by early and persistent paralysis and 
atrophy of the muscles whose nerve supply comes from the affected 
parts of the cord. 

Etiology. — The disease is endemic in certain regions, such as the 
Scandinavian Peninsula. In America it has occurred in repeated out- 
breaks involving more or less of the country. These outbreaks spread 
from ports of entry or from centers occupied by Scandinavian peoples. 
The disease is probably spread by persons who have come into contact 
with the sick, but who themselves have not had it. The infective agent, 
as in cerebrospinal meningitis, probably lodges in the nasal canities, 
and thence reaches the brain and cord. 

Children under five years of age constitute the great majority of 
victims, but older children or adults may suffer. The disease rarely in- 
volves more than one member of a family, and breaks out in most unex- 
pected quarters. Susceptibility' must therefore \Sijry greatly. The chil- 
dren of both rich and poor are aff'ected. 

Most cases develop during the hot summer months, and cold weather 
checks the outbreaks. 

Teething, exposure to cold, sitting on damp ground, previous acute 
infections, such as measles or scarlet fever, have been regarded as pre- 
disposing causes, but their influence is indetemiinate. 

Morbid Anatomy. — The cord is especially affected, but not infre- 
quently in fatal cases the brain also is involved. The lumbosacral cord 
is most affected and the lesions lessen toward the brain. These lesions 
include (a) congestion of the meninges and of the affected section of the 
cord, (b) perivascular infiltration, masses of small round cells surround- 
ing the vessels, and following them from the meninges into the sub- 
stance of the cord, and (3) degeneration of the nerve-cells in the 
affected portions of the cord. The degeneration aff'ects especially the 
ganglion cells of the anterior horns, but appears also in the posterior 
horns, and to a slight extent in the white matter of the cord. 



ACUTE POLIOMYELITIS 



507 



Secondary degenerations are found in nerves from the affected seg- 
ments of the cord, and the dependent muscles are markedly atrophic. 

The Infective Agent. — Recent investigations show that the virus 
of acute poliomyelitis can be passed through the finest filter, and that 
thus far it has defied detection by the microscope. It can be inocu- 
lated from man to monkeys and from one animal to another by using 
emulsions of the central nervous system. It thus closely resembles the 
virus of hydrophobia, but the exact agent of infection is still unknown. 

Symptoms. — The onset is often marked by sudden fever, 102° and 
103° F., vomiting and prostration, or these symptoms are entirely 
lacking. 

A day or two after the onset the paralysis appears, or the paralysis 
may be the first symptom. The paralysis involves one or both legs, 
or all four extremities, is usually complete at first, with flaccidity of 
the muscles and absence of reflexes. At the onset and for some time 
afterward the child may suffer pain, and cries when handled. 

The fever, if present, lasts only a few days, and the constitutional 
disturbance quickly passes. The sensory disturbance usually dis- 
appears shortly, but the paralysis remains. This is, however, always 
much more extensive at first than later. Recovery of power usually 
appears in the arms in a few days, if they have been affected, later 
one leg shows improvement, then the other, and in rare instances the 
paralysis wholly disappears. A more or less extensive paralysis of one 
or both legs usually remains, and even the trunk or arm muscles may fail 
to regain power. With the paralysis atrophy occurs in the affected 
parts, and becomes extreme in the muscles which remain paralyzed. 
The reflexes return after a time in the course of recovery, but remain 
absent if the paralysis is permanent. The reaction of degeneration 
develops in the paralyzed muscles. Improvement in the electrical re- 
actions, especially the return of faradic response, is significant of re- 
covery. 

The final outcome is permanent paralysis and atrophy in the muscles 
supplied from one or more spinal segments. The sensory symptoms 
always disappear early. The permanent paralysis is partial or com- 
plete, affects most often the tibial or peroneal muscles, causing per- 
manent drop-foot, but often involves the muscles of the thigh, and occa- 
sionally the trunk as well. If the thigh muscles are very weak the 
patient cannot walk without support to the knee. If the trunk is in- 
volved, the patient cannot sit up without support. 

The paralyzed limb is cold and thin, the muscles are atrophic, the 
ligaments relaxed, so that joints are abnormally movable (flail-leg). 
Secondary contractures occur and pes cavus, talipes-equino-varus or val- 
gus, and contractures at the knee or hip are common. The affected 
limb fails to grow normally, and gradually becomes shorter than its fellow. 

The duration of improvement is uncertain. Most of it is seen within 
three months ; after a year or eighteen months there is little hope for 
muscles still paralyzed. The reflexes and electrical relations are the 



508 DISEASES OF THE NERVOUS SYSTEM 



best guides to recovery. Although regaining no new power, children 
often make great progress in walking, getting about when supplied 
with adequate apparatus. 

Lumbar puncture at the onset shows an increased amount of spinal 
fluid containing an excess of lymphocytes. No organisms are discov- 
erable. 

Prognosis. — Death from acute poliomyelitis is very rare; entire 
recovery is almost as unusual. A persistent paralysis of one or more 
groups of muscles is the rule. 

Treatment. — The patients should be isolated. In cases of epidemics 
the schools should be closed. The acute stage has almost always passed 
before the diagnosis is made. Rest in bed, a light diet, a mild purge 
and care to prevent retention are indicated. Pain may require relief 
by aspirin, phenacetin or opium. For the paralysis, the limbs should 
be kept warm, passive movements practiced to prevent contractures, 
gentle friction employed, and later massage and electricity. The patient 
should be encouraged to practice and employ every movement possible. 
Later orthopedic apparatus is of great help, and in some cases graft- 
ing of nerves or tendons has been attended with success. 

ACUTE ASCENDING PARALYSIS 
(Landry's Paralysis) 

Definition. — An acute paralysis beginning in the legs and rapidly 
involving the trunk and upper extremities, usually fatal, and not char- 
acterized by definite lesions of the cord. 

Etiology. — Men between the ages of 20 and 40 years are most often 
affected; otherwise the etiology is unknown. 

Morbid Anatomy. — In his original cases Landry found no lesions 
of the cord, and the absence of gross or easily discernible lesions may be 
regarded as characteristic. Delicate microscopic changes, not discover- 
able by the methods of fifty years ago, may, however, be found in the 
spinal cord, such as breaking up or loss of the chromatin granules in 
the nerve-cells of the anterior horns and Clarke's columms, and fatty 
degeneration of the myelin sheaths of the main spinal nerves, possibly 
of the peripheral nerves. 

Symptoms.— The onset is marked by a sudden weakness, followed 
by paralysis of the legs. The muscles are flaccid. The muscles of the 
trunk, arms and neck are involved in turn. As the paralysis ascends, 
the respiratory muscles become involved, dyspnea and cyanosis result, 
and death usually ensues. In a few cases loss of power in the muscles 
of the palate, tongue and face has been observed. Apart from the 
rapidly advancing paralysis, the picture is negative. The reflexes are 
lost, but the muscles do not atrophy and the electrical reactions are pre- 
served. There are no sensory disturbances of note, and the sphincters 
are not affected. 

The duration of the disease is from two days to two weeks in fatal 



PROGRESSIVE MUSCULAR ATROPHY 



509 



cases. If recover^' occurs convalescence may be protracted. Broncho- 
pneumonia may complicate the course. 

Diagnosis. — Landry's paralysis is often confused with anterior 
poliomyelitis and acute multiple neuritis. From anterior poliomyelitis, 
the absence of other cases, the age of the patient, the absence of con- 
stitutional disturbance, the non-appearance of muscular atrophy and 
the preservation of the electrical reactions may serve to distinguish it. 
Post mortem the characteristic lesions of anterior poliomyelitis are not 
found. 

From acute multiple neuritis distinction must rest on the knowl- 
edge of a cause (such as alcoholic or metallic poisoning, etc.), the 
presence of sensory disturbances, such as pain, tingling, numbness or 
anesthesia, and muscular sensitiveness to pressure. The rarity of in- 
volvement of the trunk in neuritis (preservation of the abdominal 
reflex), and the loss of electrical reactions are significant. 

Landry's paralysis is symmetrical and complete. Multiple neuritis 
may be unevenly distributed, and some muscles may be spared. 

Prognosis. — The possibility of recovery must be admitted, but the 
usual outcome is death within a few days. 

Treatment. — There is no effective treatment. Rest in bed, a light 
diet, and regulation of the bowels are rational measures. Catheteriza- 
tion may be required. For respiratory embarrassment atropine and 
strj^chnine should be given. Frequent changes of position to prevent 
pulmonary congestion are advisable. If the patient survive, the treat- 
ment must be that of anterior poliomyelitis. 

PROGRESSIVE MUSCULAR ATROPHY 
(Chronic Anterior Poliomyelitis) 

Definition. — A progressive atrophy of muscles, usually associated 
w4th rigidity and paralysis, and due to degeneration of the motor 
neurons of the cord. 

Etiology. — The disease belongs to adult life and to men rather than 
women (five to one). Beyond these facts the causation is unknown. 

Morbid Anatomy. — The cord appears normal, but microscopic ex- 
amination shows progressive atrophy in the cells of the anterior horns 
and the central gray matter of the cord. The cells become small and 
shrunken, and many disappear. There are no signs of inflammation 
or degeneration. The axones and dendrites of these neurons likewise 
shrink and disappear. In the affected muscles there is simple atrophy 
of the muscle fibers. The atrophic process may be found at any level 
of the cord. It is usually most marked in the sacral region. 

Symptoms.- — The disease is chronic in type, lasting many years. The 
affected muscles become weak, then paralyzed, and more or less rigid. 
Fibrillary twitehings and cramps are common in them. There are no 
sensor}^ or trophic disturbances. Several types of the disease depend- 
ing upon the parts of the cord affected are described. 



510 



DISEASES OF THE NERVOUS SYSTEM 



1. Peroneal type. The paralysis begins in the peroneal muscles, 
then affects the anterior tibial group. Weakness in walking and drop- 
foot result. Gradually the process advances into the muscles of the 
thigh, the adductors and glutei. Walking becomes more difficult and 
going .up-stairs or rising from a chair may be impossible. The weak- 
ness and atrophy go steadily on till walking can no longer be accom- 
plished. Sensation is normal. There is no edema, nor bed sores. 
Bladder and rectum are unaffected. 

2. Ascending type. (Duchenne.) The muscles of the trunk are 
also involved. The patient cannot sit upright. The hands and shoul- 
ders become affected, as in the following type, and the condition ends, 
in bulbar palsy. 

3. Aran-Duchenne type. The paralysis and atrophy begin with 
the muscles of the thenar and hypothenar eminences of the hand. 
Weakness is felt in writing, in buttoning garments and the like. 
Later the lumbricales and interossei atrophy and the whole hand appears 
thin. 

Contractures give the hand the attitude of ''main en griff e" or of 
claws. One hand is affected after the other, then atrophy appears in 
the shoulders and the deltoid, biceps, brachialis anticus and other shoul- 
der muscles are involved. 

Some muscles escape the atrophy, and these by contrast appear 
hypertrophic. 

Finally the intercostals and other muscles of respiration are in- 
volved, and respiration becomes wholly diaphragmatic. 

The terminal stage is marked by involvement of the muscles of the 
face, tongue and throat, giving rise to bulbar paralysis (q. v.). The 
patients usually die of intercurrent disease. Life may be protracted 
for many years (two to twenty-five). 

The muscles gradually lose their electrical reactions, and in the 
end make no response to either galvanic or faradic currents. The re- 
flexes are similarly lost as the muscles concerned atrophy. 

Diagnosis. — Progressive muscular atrophy must be distinguished 
from the following: 

1. Amyotrophic lateral sclerosis, by the presence of exaggerated 
knee-jerk's, Babinski's reflex, and increased tendon reflexes in the arms^ 
also by some spastic rigidity in both arms and legs. The progress in 
this condition is more rapid. 

2. Muscular dystrophy, characterized by appearances of hyper- 
trophy, a different grouping of the muscles affected, and the absence 
of fibrillary twitchings. 

3. ]\Iultiple neuritis, marked by sensory symptoms, tenderness along 
the nerve-trunks, short and rapid course, and some definite causation, 
such as lead or alcoholic poisoning. 

4. Syringomyelia, early presenting like symptoms, but later develop- 
ing characteristic dissociation of sensation (loss of response to heat and 
cold, with maintenance of pain sense), and trophic changes. 



GLOSSO-LABIO-LARYNGEAL PARALYSIS 511 



The PROGNOSIS is always unfavorable, but life may be prolonged 
indefinitely. 

Treatment. — The general nutrition must be maintained by atten- 
tion to diet, fresh air, and general hygiene. Massage and rubbing may 
be employed. Electricity appears to be useless. Strychnine, and 
arsenic may be given as tonics. 

GLOSSO-LABIO-LARYNGEAL PARALYSIS 
(Progressive Bulbar Palsy) 

Definition. — ^A progressive paralysis and atrophy of the muscles 
of the tongue, lips and larynx. 

Etiology. — The disease commonly develops in late adult life, ap- 
parently as the result of exhaustion of the motor centers of the pons. 
A few early cases, probably due to congenital deficiency, have been 
recorded. No satisfactory explanation of the disease has been given. 

Morbid Anatomy. — Degeneration of the nuclei of the hypoglossal, 
glossopharyngeal, pneumogastric and spinal accessory nerves is marked. 
Many of the cells disappear. In rare cases the nuclei of the seventh 
and fifth nerves are involved. The lesions of amyotrophic lateral sclerosis 
are often associated ; some writers say they are always present. Atrophy 
of the muscles of the lips, tongue, pharynx and larynx can be shown. 

Symptoms. — A slowly progressive loss of power in the affected 
muscles is shown by difficulty in speech, in mastication and deglutition, 
in the movements of the tongue, in swallowing and phonation. Diffi- 
culty is first noted in the pronunciation of the labials and dentals 
p, b, 1, m, n, d, g, k, v, s, t. The lower lip droops and saliva escapes. 
Food collects between the lips and the gums, chewing becomes difficult 
and swallowing impaired, so that fluids regurgitate through the nares. 
The tongue cannot be protruded, and finally the voice fails. If the 
facial nerve is involved, the face loses expression. Involvement of the 
pneumogastric causes dyspnea and rapid heart-action. The patients be- 
come emotional, laughing or crying on slight provocation. 

Atrophj^ and fibrillary tremor appear in the lips and tongue. The 
affected muscles give the reaction of degeneration. Death after one 
or two years results from inanition or bronchopneumonia (aspiration). 

Diagnosis. — Th^ combination of atrophy, fibrillary tremor, and 
paralysis of the lips, tongue, pharynx and larynx, and slow, progressive 
course are characteristic. The signs of amyotrophic lateral sclerosis, 
exaggerated reflexes, spasticity and weakness in the extremities are 
usually present. Bulbar tumors or hemorrhage do not produce sym- 
metrical lesions. Myasthenia gravis shows no atrophy, no reaction of 
degeneration, and displays the characteristic early exhaustion on effort. 

A pseudo-bulbar paralysis may result from lesions of the facial 
centers in the cortex or the motor neurons leading from them (internal 
capsule), but without atrophy, tremor or degeneration. 

Bulbar palsy may form the terminal stage of either amyotrophic 



512 



DISEASES OF THE NERVOUS SYSTEM 



lateral sclerosis, locomotor ataxia, syringomyelia, or chronic anterior 
poliomyelitis. 

Treatment. — Attention to the diet, giving such easily digestible 
foods as can be swallowed, or feeding by gavage, is of help. No known 
treatment influences the underlying process or checks the disease. 

LOCOMOTOR ATAXIA 
(Tabes Dorsalis. Posterior Spinal Sclerosis) 

Definition. — A chronic disease of the sensory neurons resulting in 
incoordination, sensory and trophic disturbances. 

Etiology. — Locomotor ataxia is a disease of adult life, of men rather 
than women, a sequel of syphilis in from 50 to 90% of all cases. Trau- 
matism, such as blows or falls on the back, exposure to cold or 
wet, or exhaustion from overexertion or underfeeding are predisposing 
causes. 

Morbid Anatomy. — The lesions are found in the ganglia of the 
spinal nerves and in the fibers leading from them into the spinal cord. 
They begin and are most marked in the lumbar segments of the cord 
and develop later, and to a less extent upward. The lesions consist in 
a degeneration of the nerve-fibers and a secondary increase in the inter- 
stitial tissue. Theoretically the lesions of the ganglia should precede 
those of the nerve-fibers leading from them, but this is not always the 
case, and the sclerosis of the fibers leading from the ganglia into the cord 
— that is, the posterior columns — is the most pronounced feature of 
the lesion. The columns of Goll and Burdach are converted into dense 
connective tissue with degeneration and disappearance of the nerve- 
fibers. 

The lesions may be more widespread and involve the columns of 
Lissauer and Clark. In rare cases the process progresses upward, and 
the ganglia of cranial nerves, the hypoglossal, glossopharyngeal, the 
facial and even the fifth nerve have been found involved. 

In still rarer instances the sclerosis spreads into the anterior columns 
of the cord, producing motor symptoms. 

Symptoms. — The cardinal symptoms of locomotor ataxia include: 
(1) Pains and paresthesia, usually in the legs. (2) Bladder disturb- 
ances. (3) Ataxia of the lower extremities, rarely of the upper. (4) 
Girdle sensation. (5) Sexual weakness. (6) Weakness of vision or 
double vision. (7) Visceral crises. (8) Trophic disorders. 

The cardinal physical signs are: (1) Loss of deep reflexes, especially 
the patellar and Achilles reflexes. (2) Argyll -Robertson pupil, reac- 
tion of the pupil to light, but not to accommodation. (3) Romberg's 
sign, swaying of the body when the feet are put together and the eyes 
closed. (4) Atrophy of the optic nerve or paralysis of ocular muscles. 
(5) Areas of anesthesia, corresponding to certain spinal segments. 

The evidences of the disease develop slowly in the course of montlis 
or years. The exact grouping of the symptoms and signs varies in 



LOCOMOTOR ATAXIA 



513 



different cases. convenience of description the course may be 

• described in stages. 

1. Preataxic stages. Paresthesia and pain in the lower extremities 
in most cases mark the onset. Tingling, numbness, burning, formica- 
tion, sensations of cold, or of walking on cotton or on pins, may be com- 
plained of. Pain is usually sharp, lancinating in character, lightning- 
like, either deep or superficial, and occurring in attacks. 

The girdle sensation is a form of hyperesthesia leading to the sensa- 
tion of a band or girdle tied about the body. As the disease advances 
upward the level of the girdle or band rises, and it may be felt about 
the neck. 

Attacks of pain in other parts of the body than the legs are not 
infrequent, and are associated with disturbances which are commonly 
known as visceral crises. Gastric crises, consisting in sudden attacks 
of pain in the epigastrium, accompanied by nausea and vomiting, unre- 
lated to the taking of food, are well known. Such attacks last for hours 
or days, and are relieved only by morphine. Laryngeal crises in which 
the patient is seized by sudden cough, attended with dyspnea (due to 
adductor spasm) and a sense of severe constriction of the throat, are not 
infrequent. Vesical, urethral, intestinal and rectal crises have also been 
described. Such crises may be the earliest symptoms of locomotor 
ataxia. 

The eye symptoms may be the first of the disease, the patient com- 
plaining of gradual loss of sight, of diplopia, or of strabismus. 

Examination at this stage usually discloses the absence or impair- 
ment of the patellar and Achilles reflexes, the Argyll-Robertson pupil, 
and Romberg's sign. But in the early stages one or other of these signs 
may be missing — while the presence of some of them is essential to the 
diagnosis. In the ocular cases, atrophy of the optic nerve, or paralysis 
of some of the eye muscles is present. 

2. Ataxic stage. After more or less pain, or some of the other 
initial symptoms have been present for some time, ataxia appears, 
usually in the legs, sometimes in the hands. This ataxia is due partly 
to anesthesia, partly to loss of muscular sense, and possibly to loss of 
sensation from the joints. The patient notes that when he closes his 
eyes, as in washing his face, or when he w^alks in the dark, he loses 
his balance. Romberg's sign is closely related to these disturbances. 
The gait now becomes characteristic. In walking the foot is thrown 
outward and then forward with exaggerated motion and brought down 
with a slap on the floor. The whole action is exaggerated and awk- 
ward. The feet are widely separated and the steps are unequal and 
uncertain. The patients maintain their balance and walk only with the 
aid of their eyes, and if sight is excluded they stagger or fall. This 
ataxia can be brought out by asking the patient to follow a line with 
his toe, to cross the knees, to touch one heel to the opposite knee, etc. 

Ataxia may appear in the hands, and awkwardness is shown in writ- 
ing or in buttoning the clothes. The movements of fingers and hands 
33 



514 



DISEASES OF THE NERVOUS SYSTEM 



become exaggerated and uncouth. In the late stages the simplest 
movements may be executed with difficulty. Loss of the sense of weight 
occurs at this time, and the patient becomes unable to locate the posi- 
tion of his Imibs when deprived of sight. 

With the ataxia sensation becomes blunted and then lost. Pain and 
temperature sense both suffer. The sense of pain may be much delayed 
or lost. Temperature sense is variously affected, sensibility to cold 
often being retained when that to heat is lost. On account of this loss 
of sensibility these patients may easily be burned or injured without 
their knowledge. 

Areas of axesthesia limited to the inner or outer aspects of the 
legs or more general in distribution may be shown. These anesthetic 
areas correspond not to the distribution of peripheral nerves, but to the 
segments of the cord affected. 

Trophic disturbances develop. Herpetic eruptions appear on the 
legs or body. A perforating ulcer may develop on the sole of the foot. 
The nails become ridged or faU out: the teeth may be lost. Certain 
joint lesions (Charcot joints) are especially striking. One or more 
joints, most often the knees, become enlarged and deformed with much 
thickening about the joints and possibly effusions into them, with some 
disability, but little or no pain. The joints may suppurate. The 
muscles may become atrophic. Relaxation of muscles and ligaments 
allows of excessive movement, especially at the knee or hip, the hypo- 
tonia of Fraenkel. 

Mental s^Tuptoms are seen late in some cases. Mania, melancholia 
or paresis may develop. In some cases the mental disturbance is tran- 
sitory. 

3. Paralytic stage. The patient finally becomes unable to walk, is 
bedridden, helpless. Bulbar paralysis may appear in this stage. 
Deaths occurs from cystitis or resulting pyelonephritis, from exhaustion, 
or from intercurrent disease, rarely from locomotor ataxia itself. 

Course and Prognosis. — The disease is slowly progressive — cover- 
ing a period of ten or twenty years. It may become stationary at any 
stage, and recovery is possible, although most rare. 

Diagnosis. — The emphasis in diagnosis must be put on the signs 
rather than symptoms, the loss of reflexes. Argyll-Robertson pupil and 
Romberg's sign especially. The presence of one or more of these 
signs with any of the s^miptoms justifies a diagTiosis of tabes dorsalis. 

^Multiple neuritis is distinguished by the rapidity with which symp- 
toms develop and improvement occurs, by involvement of both arms and 
legs with integrity of the bladder and rectum, the difference in the 
areas of anesthesia (corresponding in neuritis to the peripheral nerves, 
and hence being stocking or glove-like, while in tabes they correspond 
to spinal segments and cover long areas on one or the other aspect of 
the limbs) and the absence of pupillary- changes. 

General paresis may in the early stages present symptoms of tabes, 
or late in tabes evidences of general paresis are present. The order of 



LOCOMOTOR ATAXIA 



515 



development and duration of the symptoms will then be important. 
Observation for some time may be required. 

Cerebellar disease may cause ataxia, but the incoordination dis- 
appears if the patient lies down, and headache, vomiting, etc., are usu- 
ally present. 

Neurasthenia. The reflexes can be obtained by diverting the 
patient's attention or suddenly tapping the tendon, and the pupillary 
signs are absent. 

Ataxic paraplegia is identified by the spasticity of the muscles and 
the increase of reflexes. 

Syphilitic meningitis of the cord develops rapidly, and causes pain 
in the back; the knee-jerk is not lost, and the pupil reacts to light. 

The spinal fluid regularly shows an increased cellular content, mainly 
lymphocytes. It may also give the Wassermann reaction. 

Treatment. General. — Residence in a mild, equable climate is 
advantageous. The diet should be nutritious and suited to the patient's 
digestive power. Exercise must be carefully regulated to avoid ex- 
haustion, and yet the patient should be encouraged to keep up and 
about rather than to take to bed. The condition of the bladder must 
be watched and the catheter employed, if retention occurs. The dan- 
gers of infection must be borne in mind and strict asepsis practiced. 
For constipation laxatives or enemata should be employed. 

Hydrotherapy in the form of tepid douches to the spine, the tem- 
perature varying from 75° to 95° F., is of value. Tub or sitz baths of 
like temperature may be employed. Extremes of heat or cold are harmful. 

Specific treatment for all syphilitic cases should be thoroughly car- 
ried out, salvarsan being tried, and later mercury and the iodides 
given to the point of tolerance. Inunctions of mercurial ointment, 14 
dram daily, or the protiodide may be given in doses of gr. 1/6 to gr. 
% thrice daily. The iodide is given in increasing doses up to 30 to 
60 grains, three times a day. The Wassermann reaction is useful as an 
indication of the need and duration of specific treatment. 

In other cases arsenious acid or bichloride of mercury, in doses of 
gr. 1/50 of either, three times a day, may be employed. 

For the pains, analgesics, phenacetin, acetanilid or aspirin, may be 
given. In severe attacks, such as the crises, morphine is required. 

For the ataxia the educative exercises of Fraenkel are employed. 
In these the patient practices following a straight or curved line with 
his toe, taking steps of measured length, following the sides of a tri- 
angle, etc. These exercises are repeated several times daily. Grad- 
ually the patient advances to walking upstairs and more difficult move- 
ments. Patient practice improves the use of feet or hands. 

LATERAL SCLEROSIS 
Definition. — A progressive paresis and rigidity of the muscles, 
usually beginning in the legs, without sensory symptoms or atrophy, 
due to a sclerosis of the pyramidal tracts. 



516 



DISEASES OF THE NERVOUS SYSTEM 



Etiology. — The pyramidal tracts being made up of the axones of 
motor neurones lying in the cerebral cor-tex, a descending degeneration 
and secondary sclerosis result from any injury to those neurones or 
any interruption in their course. The following lesions may be found : — 

1. Cerebral lesions, such as hemorrhages, tumors or chronic inflam- 
mation. 2. Spinal lesions, such as transverse myelitis, hemorrhage or 
tumors. 3. Disease or injury of the spine, such as caries, tumors or 
pachymeningitis, compressing the cord. Secondary lateral sclerosis is 
therefore frequently seen. 

A primary'- lateral sclerosis is established, but the etiologj^ is obscure. 
The affection occurs between the twentieth and fortieth year. Syphilis 
is occasionally the cause. 

Symptoms. — A progressive disability with stiffness and a tendency 
to cramps and tremors in the legs constitute the essential features of 
the disease. The beginning is insidious and the progress slow. The 
patient early notes a slight difficulty in moving the legs. The difficulty 
may first appear on one side, but soon both legs are involved. "Walk- 
ing, going upstairs, running or any movement is attended with increas- 
ing difficulty. The muscles become rigid, cramps are frequent, and 
passive motion of the legs meets with increasing resistance, especially 
in the adductors. The tendon reflexes are exaggerated. Ankle clonus 
and Babinski's reflex are present. There are no sensory disturbances 
of note, no atrophy, no change in electrical reactions. The loss of 
power slowly increases. The gait becomes characteristic. The patient 
takes short steps, throwing one foot around the other on account of the 
tendency to overlapping due to adductor spasm, the weight is borne on 
the ball of the foot and the heel scarcely touches the floor. Clonus may 
be excited by the touch of the toes on the ground. Gradually the power 
of walking is lost and the patient becomes bedridden. The legs then 
become flexed until the heels may touch the buttocks, and so rigid that 
they cannot be drawn down. The slightest touch excites reflex con- 
traction and tremors in the muscles. Atrophy from disuse may follow. 

The condition is very chronic, enduring for twenty or thirty years. 
Death results from intercurrent disease. Even in advanced cases the 
hands are rarely affected. 

Diagnosis. — The symptoms and signs of lateral sclerosis are easily 
recognized. That the disease is primary can be affirmed only by the 
exclusion of the many causes for the secondary condition. Hysteria 
must be excluded. 

Treatment of the primary type is wholly palliative. Division of 
the posterior roots of the spinal nerves supplying the affected muscles 
has been employed with some relief. In the secondary cases the primary 
condition must be treated. 

HEREDITARY SPASTIC SPINAL PARALYSIS 
Definition. — A spastic spinal paralysis, occurring in families, 
due to lack of development or degeneration of the pyramidal tracts. 



ATAXIC PARAPLEGIA 



517 



Etiology. — Beyond the fact that the affection develops in several 
members of a family, nothing of value is known. 

Morbid Anatomy. — Degeneration of the pyramidal tracts through- 
out the cord, but especially in the lumbar region, is found. Occasion- 
ally the degeneration involves neighboring tracts, such as the direct cere- 
bellar and the column of Goll. 

Symptoms. — These are those of lateral sclerosis, as given above. 
The symptoms appear in the first year or in adult life. Some patients 
develop symptoms rapidly, some slowly. The hands are rarely affected. 
The familial occurrence is the only distinctive feature of these cases. 

Diagnosis. — Secondary lateral sclerosis must be excluded. The 
occurrence of other cases in the family is the only clue to the hereditary 
nature of the affection. 

Treatment is that of lateral sclerosis. 

ATAXIC PARAPLEGIA 

Definition. — A sclerosis of the posterior and lateral columns of the 
cord, producing spastic paraplegia with ataxia. 

Etiology. — Middle-aged men are most often affected. Injury or ex- 
posure may precede the onset. 

Morbid Anatomy. — A sclerosis of the lateral pyramidal and the 
adjacent portions of the posterior columns is found. 

Symptoms. — The patient suffers from progressive weakness in the 
legs, together with unsteadiness of gait and lack of coordination in the 
movements remaining. No pain or other sensory symptoms develop. 
The reflexes are exaggerated, and the spasticity, cramps and tremor of 
lateral sclerosis appear. The sphincters are not involved and the eye 
symptoms appear late. 

FRIEDREICH'S ATAXIA 
(Marie's Hereditary Cerebellar Ataxia) 

Definition. — A combined sclerosis of the posterior nerve-roots, the 
posterior and lateral columns, producing ataxia and paraplegia. 

Etiology. — The disease occurs in several members of a family, 
apparently owing to some congenital defect. Alcoholism, tuberculosis, 
or syphilis in the parents predisposes to it. A neuropathic tendency 
shown by the occurrence of migraine, epilepsy, hysteria, or insanity is 
often found in the family. Trauma of any kind, an acute infectious 
disease, or any influence lowering the vitality of the patients favors the 
development of the disease. 

Morbid Anatomy. — The cord is smaller than normal, the atrophy 
affecting especially the posterior columns. On section a sclerosis is 
found involving the columns of Goll and Burdach, the direct cerebellar 
tract, and the antero-lateral tract of Gowers. The pyramidal tracts, 
especially the crossed, are affected in some degree. The cells in the 
column of Clarke are degenerate. 



518 



DISEASES OF THE NERVOUS SYSTEM 



Symptoms. — The disease appears early, before puberty as a rule. 
Ataxia of the lower extremities is first noted. The child walks mth 
feet wide apart, bringing the foot down with a stamp, balancing him- 
self by the aid of the hands, like an intoxicated person. Romberg's 
sign may be present. The knee-jerks are lost; Babinski's reaction pres- 
ent. Gradually the ataxia affects the upper extremities, leading to 
awkrsvard movements, suggesting chorea. Swaying movements of the 
body and head develop. The muscles of the trunk are weakened and 
the spine appears scoliotic. 

Contractures of the muscles of the extremities produce talipes equino- 
varus and other deformities. Speech becomes slow and jerky and 
nystagmus is present. The mind remains clear. The muscles of the 
extremities are atrophic and electric excitability is diminished. 

Cerebellar type. Marie and others have described a cerebellar type 
in which with the ataxia the patellar reflexes are retained, the legs be- 
come spastic. Lancinating pains may occur in the early stages, but 
sensory or trophic disturbances are absent in both. 

Course. — The disease is progressive, the patients are finally bed- 
ridden, but may survive twentj^ or thirty years. 

Treatment is that of locomotor ataxia. 

SYRINGOMYELIA 

Definition. — A chronic disease of the spinal cord, characterized path- 
ologically by the presence of one or more abnormal cavities in the cord, 
and clinically by dissociative anesthesia, trophic disturbances and pro- 
gressive muscular atrophy and paralysis. 

Etiology. — The disease develops between twenty and forty years, in 
men more often than in women. The patients often present defects of 
development, such as infantilism, bosses on the skull and spina bifida 
occulta. Trauma of the head or spine may precede the onset. 

Morbid Anatomy. — The essential feature is the presence in the 
cord of one or more pathological cavities. Externally the cord appears 
normal, or may be enlarged and fluctuating in some part, if the ca^-ity 
is large. On section the cavity is found, usually in close relation to 
and communicating with the central canal, more often involving the 
posterior parts of the cord. The cavity is rarely symmetrical, one side 
being, as a rule, decidedly more affected, but the cavity may be of any 
shape or size, so that it may replace almost the whole area of the cord, 
leaving only a shell-like remnant. 

The length of the cavity also varies greatly, involving in some cases 
only two or three segments, and in others the whole length of the cord. 
The cavity rarely extends into the brain, but has been seen to extend to 
the fourth ventricle, or even the internal capsule. 

The contents of the cavity are clear serum; its wall is made up of 
thickened neuroglia tissue. In some parts the cavity is lined with 
epithelium apparently from the central canal, with which the ca^sity 
often communicates. If a large area of the cord is involved there may 



SYRINGOMYELIA 



519 



be secondary ascending and descending degenerations from the level of 
greatest destruction. 

The pathogenesis of syringomyelia is thus far undetermined. Sev- 
eral explanations are offered. (1) Congenital defects of development. 
(2) A primary increase in neuroglia tissue (gliosis) due to inflamma- 
tion, with secondary degeneration of the cord. (3) Interference with 
circulation due to vascular changes, which determines the degeneration. 
(4) Intramedullary hemorrhage with like result. 




Fig. 104. — Atrophy and anesthesia in syringomyelia, front view. (International Clinics, Vol. II, Series 

20, page 219.) 

Symptoms. — The patient complains of increasing weakness and 
atrophy in some part, usually the hand and arm, or of pains and 
paresthesia (tingling, numbness, heat or cold). 

The characteristic conditions are found on examination, and include: 
(1) Dissociative anesthesia, the sense of touch being preserved while 
those of pain and temperature are lost. (2) Trophic disturbances of 
greater or less extent. (3) Atrophy and paralysis of some muscles. 
With these may be combined many other disturbances of the functions 
of the cord, depending upon the extent of the involvement of its sub- 



520 



DISEASES OF THE NERVOUS SYSTEM 



stance. The evidences of syringomyelia are usually most marked on 
the upper extremities and trunk, but may first appear on the lower. 
Both sides are commonly involved, but one to a greater extent than the 
other. The areas of anesthesia, paralysis or atrophy while overlap- 
ping do not correspond to one another. If the entire area of the cord 
is involved at any level, the evidenices of lateral sclerosis in the cord 
below that point appear. (See Figs. 104 and 105.) 




Fig. 105. — Atrophy and anesthesia in syringomyelia, back view. (International Clinics, Vol. IT, Series 

20, page 219.) 

1. Sensory Disturbances, (a) Thermo-anesthesia is ahnost con- 
stant. Sensation to both heat and cold is usually lost, but one may be 
preserved. The area involved may be small or large, and corresponds 
to certain spinal segments, not to the distribution of peripheral nerves, 
(b) Analgesia is usually present with thermo-anesthesia. (c) Tactile 
sensibility is long preserved, but may be lost in the final stages, (d) 
Pain or paresthesia may mark the onset. The pain may be severe. 

2. Motor Disturbances, (a) Paresis or paralysis ordinarily ap- 
pears in the hand. Atrophy accompanies it. The muscles of the hand 
or arm may be much wasted. Contractures may give the appearance 



SYRINGOMYELIA 



521 



of "main en griffe." The paralyzed muscles may show fibrillary 
tremors and the reaction of degeneration, (b) Spastic paralysis, loss 
of power without atrophy or degeneration and with increased reflexes, 
may appear below the level of most marked cavity formation. This 
spastic paralysis naturally appears most often in one or both legs, but 
may involve the upper extremities as well, (c) Spinal curvature or 
scoliosis, resulting from muscular inequalities, is quite common. It is 
most marked in the dorsal portion of the column, (d) Ataxia may be 
quite marked. 

3. Trophic Disturbances, (a) Skin. Atrophy of the skin with 
eruptions of vesicles or bullae is common. The skin becomes glossy, 
thin and cracks or fissures appear. Ulceration may follow, necrosis 
of bone develop and whole parts (fingers or toes) be destroyed. The 
nails are thickened and brittle; they may drop off. (b) Bones. Ne- 
crosis occurs in some cases. Hypertrophy or atrophy and spontaneous 
fracture are occasionally seen, (c) Joints. Arthropathies are fre- 
quent (25% of cases). The shoulder or elbow is most often involved; 
other joints may suffer. The changes are the same as those seen in 
locomotor ataxia (Charcot joints), thickenings, deformity, effusions, 
with destruction of the articular surfaces or the heads of the bones in 
some cases. These arthropathies are usually painless. 

4. Vasomotor and Secretory Disturbances. Pallor or hyperemia or 
cyanosis, dryness or excessive sweating is frequently observed. 

5. Accessory Disturbances, (a) Ocular symptoms. Owing to fre- 
quent involvement of the last cervical and first dorsal segments, pupil- 
lary and ocular symptoms are seen in the great majority of cases. The 
pupil is smaller, the palpebral fissure narrower and the eyeball is some- 
what retracted. These affections give a suggestion of ptosis, Avhich is 
promptly proven false, when the patient looks upward, (b) Bulbar 
symptoms appear late in the disease. Atrophy and tremor of the tongue, 
paralysis of vocal cords, difficulty in swallowing or in respiration may 
occur, (c) Sphincteric control. In the usual (dorsal) type of the dis- 
ease, disturbance appears late. If the lumbo-sacral cord is affected at 
the outset, these disturbances appear early. 

Course. — The disease is usually far advanced when recognized. It 
progresses slowly, but surely. Death after some years occurs from 
cystitis and its complications, from exhaustion due to bed sores and 
suppuration, or suddenly from rupture of the cord. 

Diagnosis. — Syringomyelia in typical form is easily recognized, but 
easily overlooked in irregular types. The diagnosis depends mostly on 
thorough examination, which elicits the analgesia and disturbances of 
thermic sensibility. These and the trophic disorders distinguish the 
disease from chronic anterior poliomyelitis, progressive muscular 
atrophy or amyotrophic lateral sclerosis. 

The asymmetry of the lesions of syringomyelia and the preserva- 
tion of the sense of touch distinguish it from myelitis, transverse or 
disseminated. Tumors of the cord may give a like history, but regu- 



522 



DISEASES OF THE NERVOUS SYSTEM 



larly cause severe pain, are steadily progressive, are limited to two 
or three segments of the cord, and cause symptoms of a transverse 
myelitis below the level of location. 

Prognosis. — The disease is incurable, but very chronic. It often 
becomes stationary. Treatment must be symptomatic. Care must be 
taken to avoid burns or injuries. Paralysis must be treated as in 
anterior poliomyelitis. 

Morvan's disease is a type of syinngomyelia in which trophic 
changes are very prominent. Pains and atrophy develop in the hands, 
with analgesia and anesthesia, and are followed by painless felons and 
possibly necrosis of the phalanges. 

TUMORS OF THE SPINAL CORD 

Tumors of the cord are rare. They may be of almost any variety. 
Sarcoma, tubercle, gumma, fibroma, glioma, are the more conmion forms. 
These growths may spring from the cord (intramedullary) or from the 
dura covering it (extramedullary) . It must be recalled that com- 
pression of the cord is much more frequently the result of pressure 
due to caries of the vertebrae, or tumors growing in the vertebras (sar- 
coma, carcinoma, myeloma), than of the pressure of tumors of the cord 
itself. 

Etiology. — Tumors of the cord are more common in adult life, but 
may develop in childhood. (One in three under the age of sixteen.) 
Except for syphilis or tubercle, we can give no satisfactory causation. 

Morbid Anatomy. — The tiunors are of great variety. The most 
common site is the dorsal cord, but any part may be involved. Apart 
from the tumor itself the cord shows the effects of compression, or a 
nwelitis may be set up. 

Symptoms. — These are caused by pressure upon the cord, gradually 
increasing till the functions of the cord at the level of compression are 
destroyed. The sjanptoms are those of compression (page 505), but 
with certain fairly distinctive features. Pain is severe, neuralgic in 
character, intense, at first unilateral and sharply localized, but after a 
time spreading to the other side. The painful area is hyperesthetic. 

At the level of the tumor there are atrophy and paralysis of mus- 
cles with reaction of degeneration, anesthesia of the skin, herpes zoster 
and trophic changes. Dissociative anesthesia (preservation of touch 
with loss of sensibility to pain and temperature) is suggestive of an 
intramedullary growth. 

Below the level of the gro"s^i:h weakness with exaggerated reflexes, 
imperfect control of bladder and rectum, loss of sensation up to the 
level of the lesion, and a tendency to bed sores are developed. 

The course varies with the nature of the tmnor, but the average 
duration of life is less than two years. 

Tumors of the cauda equina cause severe sacral pain and unusually 
^Wdespread pain in the nerves of the legs. Paralysis and atrophy may 
be limited and are rarely symmetrical. Paralysis of bladder and rec- 
tum occurs early. 



DISEASES OF THE MENINGES 



523 



Diagnosis. — Caries of the spine from any cause must be excluded. 
Eigidity of the spine, tenderness over the spinous processes, increase 
of pain on motion or walking, and kyphosis must be sought for. A 
radiograph of the spine is valuable. The nature of the tumor is diffi- 
cult to determine. Fever and other constitutional disturbances, and 
evidences of disease elscAvhere, are found in tuberculosis. In syphilis 
the history is important, the presence of other lesions, or a Wassermann 
reaction helpful. An antecedent malignant tumor is suggestive. 
Otherwise we can only hazard a guess at the nature of the tumor. 

Prognosis is unfavorable. Surgical removal of the tumor may be 
successful. 

Treatment. — In specific cases active anti-syphilitic treatment is in- 
dicated. In other cases if the tumor can be reasonably localized, opera- 
lion should be undertaken, unless the tumor is known to be malignant. 

DISEASES OF THE BRAIN AND MENINGES 

DISEASES OF THE MENINGES 

EXTERNAL PACHYMENINGITIS 

Definition. — An inflammation of the external layer of the dura 
mater. 

Etiology. — Fractures or disease of the bones of the skull (caries 
following middle-ear disease and the like), syphilis, or tumors involv- 
ing the bones, may be the cause. Erysipelas occasionally causes an 
acute inflammation. 

Morbid Anatomy. — The dura is thickened, unusually dense and 
adherent. An accumulation of pus or blood may be found between it 
and the bone. 

Symptoms. — The condition is often unexpectedly found at autopsy, 
especially in the insane. The symptoms are those of the primary trou- 
ble, with persistent headache and local tenderness. 

Treatment. — Syphilitic disease should receive specific treatment. 
Otherwise the treatment must be directed to the cause. If pus is pres- 
ent, trephining must be done. 

INTERNAL PACHYMENINGITIS 

Definition. — An inflammation of the internal surface of the dura 
mater. 

Etiology.— It may be part of an external pachymeningitis and arise 
from the causes of that condition. It is common in the insane. Sun- 
stroke, alcoholism or syphilis and various wasting chronic diseases are 
regarded as causative. 

Morbid Anatomy. — The dura is thickened and its inner surface is 
covered with a layer or layers of delicate connective tissue unusually 
rich in blood-vessels. The I'upture of these vessels gives rise to re- 
peated hemorrhages, which in turn organize and increase the thick- 
ness of the membrane. The brain may be compressed. 



524 



DISEASES OF THE BRAIN AND MENINGES 



Symptoms. — Often no symptoms are presented. Headache, slight 
difficulty in memory or in thinking may be present for years. With 
the recurrent hemorrhages the patient may have repeated attacks of 
hemiplegia or monoplegia. The recurrence and rapid disappearance of 
apoplectic attacks are suggestive. With extensive hemorrhage convul- 
sions or coma may be produced. 

Treatment must be directed to the cause, if ascertainable. 

ACUTE LEPTOMENINGITIS 
(Acute Meningitis) 

Definition. — An acute inflammation of the pia-arachnoid of the 
brain and spinal cord. The inflammation is, in rare instances, limited 
to the cerebral or spinal membrane, but in the great majority of cases 
the entire membrane is involved. 

Etiology. — Acute meningitis is regularly of bacterial origin. The 
bacteria capable of causing meningitis are of many varieties, the diplo- 
coccus intracellularis, the tubercle bacillus, the pneumococcus, strepto- 
cocci, staphylococci, the typhoid and influenza bacilli, the spirochete 
of sj^philis. Certain of the infecting organisms cause a meningitis so 
distinctive in its symptomatology and course as to merit description 
separately. The diplococcus intracellularis is the cause of epidemic 
cerebrospinal meningitis. The tubercle bacillus gives rise to a dis- 
tinctive clinical condition. Syphilitic meningitis requires separate con- 
sideration. 

The meningitis excited by the pneumococcus, streptococci or 
staphylococci, the influenza or typhoid bacilli may be considered together 
as a suppurative meningitis. 

1. CEREBROSPINAL MENINGITIS 
(Cerebrospinal Fever. Spotted Fever) 

Definition. — A specific infectious disease, caused by the menin- 
gococcus, occurring sporadically and in epidemics, and marked by in- 
flammation of the meninges of the brain and cord and by severe nervous 
symptoms. 

Etiology. — A few sporadic cases are met with every year in almost 
all of the larger cities. In addition, epidemics, sometimes of consider- 
able extent, are not infrequent both in country and town. These occur 
almost always in the late winter and spring. Overcrowding, filth, poor 
food and fatigue are predisposing causes, and yet the disease appears 
at times among the children farthest removed from these conditions. 
Children and young adults are chiefly attacked. 

The direct cause is a specific micro-organism — the diplococcus 
INTRACELLULARIS MENINGITIDIS of Wcichselbaum — which is found 
abundantly in the inflammatory exudate and especially in the bodies 
of the pus cells. In size and shape it much resembles the gonococcus. 



DISEASES OF THE MENINGES 



525 



This germ has been found in the nasal secretion, and it is probable that 
infection of the meninges occurs through the ethmoidal cells. The 
disease is directly contagious, but susceptibility varies and communi- 
cation can rarely be established. 

Morbid Anatomy. — There is an acute exudative inflammation of the 
pia-arachnoid of the brain and spinal cord, the exudate consisting of 
serum, fibrin and pus in varying proportions. In the rapidly fatal 
cases an intense hyperemia may be the only visible sign of inflamma- 
tion. Usually, however, turbid serum or pus may be seen abundantly 
over the vertex and base of the brain, especially in the sulci. The 
exudate is usually very abundant over the posterior surface of the dor- 
sal and lumbar cord. The inflammation also involves the superficial 
layers of the brain and cord, and regularly extends to the sheaths of 
the cranial and spinal nerves. The ventricles of the brain are often 
distended with turbid fluid. In some of the chronic cases the men- 
inges become opac[ue and thickened. There are no characteristic lesions 
of the other viscera. 

2. TUBERCULOUS MENINGITIS, ACUTE HYDROCEPHALUS 
Tuberculous meningitis is always secondary to tuberculosis else- 
where in the body, and is usually only a part of a general miliary tuber- 
culosis in which symptoms referable to other organs are overshadowed 
by those of the meninges and brain. The disease is much more com- 
mon in children than in adults. Foci of tuberculosis in the bronchial 
or mesenteric lymph-nodes, bones, joints, lungs, etc., are the sources of 
general infection, but it frequently happens that the primary focus 
is not demonstrable during life. Sometimes a fall or an injury may 
seem to be the exciting cause. 

Morbid Anatomy. — The inflammation is confined chiefly to the pia 
mater of the base of the brain (hence the name basilar meningitis), 
and consists not only of an eruption of tubercles but of more or less 
fibrino-purulent exudate as well. The tubercles are most abundant in 
the interpeduncular space and in the Sylvian fissures, and are apt to 
lie in close relation to the arteries. Often they are so small as to be 
seen only with difficulty ; sometimes they extend for some distance 
down the membrane of the cord and over the lateral surfaces of the 
hemispheres. The lateral ventricles are often distended with fluid 
(acute hydrocephalus) and the convolutions correspondingly flattened. 
The inflammation frequently extends from the pia to the subjacent 
cerebral cortex. 

3. ACUTE SUPPURATIVE MENINGITIS 
Etiology. — Acute suppurative meningitis is nearly always a sec- 
ondary process. In rare cases the primary process is so slight, a bron- 
chitis for example, that the meningitis appears to be primary. Three 
chief groups of cases are recognized. (1) Meningitis secondary to 
local infections, such as otitis media or mastoid disease, suppuration of 



526 DISEASES OF THE BRAIN AND MENINGES 



the nasal or ethmoidal sinuses or the orbit, infected fractures of the 
sknll, especially fractures involving the middle ear or the nasal 
passages, abscess of the brain, bed sores or other suppurative processes 
in proximity to the spinal canal. (2) Meningitis secondary to sys- 
temic infections, such as pneumonia, infective endocarditis, septicemia 
or pyemia, typhoid fever or influenza, and various other acute infective 
diseases, such as measles, small-pox, rheumatic fever, actinomycosis and 
anthrax. (3) A terminal meningitis occurring as a rare complica- 
tion of chronic nephritis, arteriosclerosis, gout and the wasting diseases 
of children. 

Of these three types the first is by all means most important be- 
cause it is to some extent preventable or remediable by proper treat- 
ment of the primary condition. 

Morbid Anatomy. — The pia mater is congested and presents a 
more or less extensive exudate of fibrin, serum, and leukocytes. The 
exudate is most abundant along the vessels and in the sulci. It infil- 
trates the membrane, making it opaque and giving it a yellowish or 
greenish yellow color. In many cases the exudate is most abundant 
at the base of the brain, over the pons and the adjacent structures; in 
other cases the vertex is covered and the base free. If very extensive, 
almost the entire surface may be covered. The cerebrospinal fluid be- 
comes more abundant than normal and turbid or purulent by admix- 
ture with the inflammatory exudate. The pia mater of the cord regu- 
larly shows the same conditions as that of the brain. 

In meningitis resulting from extension from a local focus such as 
otitis media, the adjacent pia mater shows the most extensive changes, 
and the micningitis may be closely limited. 

Cerebral Changes in jMeningitis. — In any meningitis the under- 
lying brain shows some inflammatory or degenerative changes. Con- 
gestion, edema and degeneration of the nerve-cells are common; an exu- 
date of leukocytes may be found especially along the vessels. 

The SYMPTOMS of meningitis are conveniently grouped into three 
stages, although these are by no means always well deflned. In tuber- 
cular cases, there is, beside, a prodromal period of some days or even 
weeks during which the child feels out of sorts without being distinctly 
ill. The disease begins usually with headache, vomiting and fever as 
the chief symptoms. Sometimes it may be ushered in by convulsions. The 
headache is persistent and very severe ; the vomiting is without appar- 
ent cause; the fever is usually not high (100° to 103° P.). There are 
great irritability and restlessness, and sometimes active delirium. The 
neck becomes rigid and the head retracted; the pupils are contracted: 
there may be twitching or rigidity of the extremities. Even when un- 
conscious the child frequently utters periodically a short, hoarse cry 
— the so-called hydrocephalic cry." The neck is rigid; Kernig's sign 
is present, i.e., with the thigh flexed at 90° on the pelvis the leg cannot 
be completely extended; Babinski s reflex, hyperextension of the great 
toe, when the inner border of the foot is gently scratched, and the phe- 



DISEASES OF THE MENINGES 



527 



nomena shown in Figs. 106 and 107 may be demonstrated. This initial 
period is called the stage of irritation or excitement, and lasts only a 
few days. 

The second stage, that of depression, is marked by a gradual relief 
from the intolerable headache, and a change from irritability and rest- 
lessness to drowsiness and stupor. The irregular temperature con- 
tinues ; the pulse is often slow or irregular ; there is obstinate constipa- 
tion and the belly is usually retracted and boat-shaped. Local paralyses 
of the eye, face or extremities may occur, or there may be muscular 
twitchings or rigidity. Kernig's sign is present. Vasomotor disturb- 
ance is shown by the frequent presence of the so-called tache-cerehrale 
— a distinct white streak bounded by a reddish flush, which appears 
where the finger-nail is drawn over the skin. A moderate grade of optic 
neuritis is common. In the terminal stage of paralysis stupor merges 
into deep coma; the sphincters are relaxed; the reflexes abolished; the 
pupils widely dilated, and the pulse grows very rapid and feeble. There 




Fig. 106. — Contra-lateral reflex in meningitis. Flexion of one leg causes like flexion of the other. 
Fig. 107. — Identical reflex in meningitis. Flexion of the neck causes flexion of the arms and legs. 
(Brudzinski. ) 



may be local paralyses, hemiplegia or general muscular relaxation; the 
temperature falls to subnormal or rises rapidly, and the patient dies in 
convulsions or in deep coma. The active stage of the disease commonly 
lasts from two to four weeks. It may, however, be fatal within a week 
or may extend over two or three months. 

Recovery is rare, and only a very few well authenticated cases are 
recorded. 

Special Features of Cerebrospinal Meningitis. — Symptoms. 
— The incubation period is probably less than one week. The onset is 
usually sudden and violent. The symptoms presented are those enumer- 
ated under meningitis with few important differences. In the average 
case the fever is higher and the course more acute than in tubercular 
meningitis. Certain rashes appear in the epidemic type, (a) Herpes 
labialis is very common, (b) A petechial rash appears in some cases, 
and more frequently in some epidemics than in others, upon the ex- 
tremities, trunk and possibly the face (spotted fever). The individual 
spots are of varying size and shape, but usually small. (See Fig. 108.) 
(c) Blebs, resembling pemphigus, occur in rare instances, and ulceration 



528 DISEASES OF THE BRAIN AND MENINGES 



or even gangrene of the skin may develop. At least 50%, and under 
serum treatment, a still higher percentage of the patients recover. 

An acute inflammation of the joints occurs in about 10% of the 
cases. 

Unusual Types of Cerebrospinal Meningitis. — The malignant 
form is marked by a violent onset, wild delirium, a very feeble pulse, 
either slow or rapid, irregular breathing, coma and death in from 
twelve hours to three days. 

In the MILD FORM mental symptoms are usually lacking, the course 
is short and the symptoms not well marked. 

Abortive cases occur in which after a violent onset the fever and 
other symptoms rapidly subside, and convalescence begins within two 
or three days. 

In the INTERMITTENT OR RELAPSING FORM febrile intervals alter- 
nate in a very irregular way with afebrile periods of several days' 
duration, during which all the symptoms abate. These periods of 
apparent recovery are very deceptive. 



Fig. 108. — The eruption of cerebrospinal meningitis. Scattered. 



The CHRONIC FORM is met with chiefly in children. The disease 
lasts many weeks or months. The child lies in stupor, emaciation 
becomes extreme, and bed sores and contractions of the limbs are 
common. 

Complications and Sequelae. — Comphcations such as pneumonia, 
pericarditis, pleurisy and nephritis are occasionally seen. Severe con- 
junctivitis and iritis are seen not infrequently. Sequelae are frequent 
and important, and include blindness, deafness, paralyses, mental weak- 
ness, aphasia, etc. 

Prognosis.— The disease is, as a rule, very fatal but the mortality 
varies greatly in the different epidemics, and may range anywhere be- 
tween 30 and 75 per cent. 

Diagnosis.— Fever, with severe headache, insomnia, delirimn and 
cerebral vomiting, should always suggest acute meningitis. The pres- 
ence of rigidity of the neck and Kernig's sign in any case render the 
dingiiosis highly probable. In employing the latter sign it is, how- 
ever, important to know that in many persons, with the thigh flexed 



DISEASES OF THE MENINGES 



529 



to a right angle, complete extension of the leg is impossible without 
some force and resulting pain. In a true Kernig's dgn complete ex- 
tension of the leg is practically impossible. 

Every added sign of meningitis, the hyperesthesia, pupillary or 
ocular signs, rigidity and paralysis, adds to the certainty of diagnosis. 

In certain acute infectious diseases, however, such as pneumonia^ 
typhoid fever, and the enteric infections of children, a condition (men- 
ingism) arises, which can with difficulty be distinguished from acute 
meningitis. This possibility must therefore be borne in mind. The 
symptoms of this condition are not progressive ; on the contrary, they 
vary from day to day and may promptly clear up. 

The Variety of Meningitis.^ — Cerebrospinal.— The presence of an 
epidemic, sudden onset, violent course (fever 104° to 106° F.), charac- » 
teristic eruptions indicate the specific type. 

Tubercular. Previous tubercular affection of bone (joints), glands, 
or lungs, a prodromal period of irritability and change of character, an 
insidious onset and rather subacute course with low fever — 100° to 
103° F. — suggest tuberculosis. A positive von Pirquet test is valuable in 
children. 

Suppurative. Knowledge of an adequate cause, a local or systemic 
infection is here of greatest moment. 

Lumbar puncture, as a rule, renders decisive information as to the 
presence and the variety of meningitis. 

Excess of fluid under pressure, its physical characters, and the 
finding of bacteria in it are the important observations. 

The normal pressure in the spinal canal amounts to 100 to 150 mm. 
of water, and the spinal fluid drips slowly from the puncture needle. In 
meningitis the pressure will often rise over 200 mm., and the fluid 
flows rapidly or even spurts from the needle. Tubercular meningitis 
usually gives a perfectly clear fluid ; cerebrospinal a clear or moderately 
turbid fluid; suppurative meningitis a turbid or purulent fluid. 

If the cells in the fluid be counted, a lymphocytosis is commonly 
found in tubercular meningitis, a polynuclear excess in the other forms, 
but many departures from this rule are observed. 

In the clear fluid of tubercular meningitis a fine coagulum forms 
in from 12 to 24 hours. On staining tubercle bacilli are found. In 
cerebrospinal meningitis the diplococcus intracellularis can be demon- 
strated, in suppurative meningitis, the pneumococcus, streptococci, 
staphylococci, or other causative bacteria. 

The blood in meningitis shows a leukocytosis, even in many of the 
tubercular cases. Still, absence of leukocytosis or leukopenia suggests 
a tubercular infection, while very high counts (over 30,000) occur only 
in cerebrospinal fever. A differential count of leukocytes may show 
a lymphocytosis in the tubercular type; in the other forms the poly- 
nuclears prevail. 

Lumbar puncture is performed with the patient lying on one side, 
the legs drawn as far up as possible and the head bent forward, to in- 
34 



530 



DISEASES OF THE BRAIN AND MENINGES 



crease the separation between the vertebrae. The patient should be 
held by an assistant or secured in this position by a sheet passed under 
the knees and about the neck. Courageous adults may be allowed to 
sit on a chair or stool, wdth the back bent forward. An aspirating 
needle, 8 to 10 cm. long and IV2 inm. caliber, may be used, or, better, 
the Quincke needles with a relatively blunt point. The needle is in- 
serted between the third and fourth lumbar vertebras (the level of the 
crests of the ilia), either in the mid line or at one side, and directed 
toward the spinal canal. The dura is pierced at a depth of from 2 
to 7 cm. The needle should be passed well in and then mthdrawn a 
little. 

Prognosis. — Tubercular and suppurative meningitis are practically 
always fatal. Recovery may occur, but is too rare to be counted upon. 
The mortality of epidemic cerebrospinal meningitis varies in epi- 
demics from 30% to 75%. Under treatment by the Flexner-Jobling 
serum, the mortality has in some series fallen to 10% to 15%. 

Treatment of Acute Meningitis. — A quiet, darkened room is re- 
quired. In the stage of irritation the patient should be disturbed for ex- 
amination or treatment only when necessary. The nutrition should be 
preserved by careful feeding, by gavage if the patient will not swal- 
low. Careful nursing wdth special attention to the bed and skin is 
necessary to prevent bed sores. An ice-cap is to be kept continuously 
on the head. 

Sedatives. Bromides, chloral or morphine may be required for the 
relief of pain in the early stages. Hot baths or packs sometimes give 
relief from restlessness and pain. 

Lumbar puncture repeated at intervals of several days, according 
to the activity of the disease, as much fluid as flows freely being with- 
drawn each time, mitigates the symptoms. 

Specific Serum for Cerebrospinal Meningitis. — The anti-menin- 
gococcus serum of Flexner and Jobling has proven its value. After 
the withdrawal of 30 c.c. or more of the spinal fluid from 30 to 45 c.c. 
of the serum are injected through the puncture needle into the subdural 
space. In the severe cases or those coming late under treatment the 
larger dose is used. The injections are to be repeated at 24:-hour in- 
tervals, as long as the specific diplococci can be found in the exudate, 
at least four doses being given. The injections should be repeated in 
relapsing cases. 

4. SYPHILITIC MENINGITIS 

Syphilitic meningitis is one of the grave results of specific infec- 
tion. It is a slowly progressive process developing in the later stages 
of the infection. The clinical picture is not that of an acute menin- 
gitis, but of brain tumor or paretic dementia. So that in either of 
these conditions syphilis must be excluded by the history, the examina- 
tion of the patient for active lesions or scars, the Wassermann reaction, 
and finally by the therapeutic test of active specific treatment. 



DISEASES OF THE MENINGES 



531 



THROMBOSIS OF CEREBRAL SINUSES AND VEINS 

Thrombosis in the cerebral sinuses may occur in chlorosis and vari- 
ous wasting* diseases without definite cause. In most cases it results 
from phlebitis caused by extension of inflammation from some adjacent 
part into the vein. Thus thrombosis of the lateral sinus follows mas- 
toid disease, that of the longitudinal sinus follows pachymeningitis, 
while disease of the nasal passages or orbit may cause thrombosis of the 
cavernous sinus. Such thromboses are usually infected and symptoms 
of pyemia result. 

Longitudinal Sinus. — The thrombus may be discovered only at 
autopsy, having given no symptoms. Venous stasis of the scalp, orbit 
and eye, nose-bleed and choked disk may result. 

Lateral Sinus. — Thrombosis here is most often a complication of 
middle ear and mastoid disease. The constitutional symptoms of pyemia 
with chills and rapid oscillations of temperature are present. The local 
signs of swelling and tenderness over the mastoid, swelling and ten- 
derness of the jugular vein in the neck, emptiness of the jugular vein 
below the thrombosis, and nystagmus may be present. 

Aphasia may be caused and there may be severe headache, vomit- 
ing and stupor, suggesting abscess of the brain. 

The sinus should be exposed through the mastoid, and after ligation 
of the vein in the neck, opened and emptied of its thrombus. 

Cavernous Sinus. — Following disease of the nasal passages or orbit, 
edema of the orbit and conjunctiva with exophthalmos develops. The 
retina may be intensely engorged. The ocular muscles may be paralyzed 
and strabismus result. Suppurative panophthalmitis may follow. 
S^Tuptoms of septicemia or pyemia accompany the process. 

Treatment must be directed to the primary condition. 

CEREBRAL ANEMIA 

Anemia of the brain is ordinarily part of a general anemia due to 
hemorrhage, chlorosis, pernicious anemia and the like. Headache, 
faintness, vertigo, loss of consciousness, or even convulsions may be 
produced by sudden severe anemia, and similar symptoms may develop 
in the chronic conditions, but it is remarkable how few symptoms, ex- 
cept unusual fatigue, the brain commonly gives in severe anemias. 

Local anemia may be produced by disease of individual vessels, 
or by the pressure of tumors or the accumulation of exudates (abscesses, 
etc.). If functionally active areas are involved, symptoms of impair- 
ment (aphasia, paralysis) may follow, but in most cases pressure 
rather than anemia explains these results. 

CEREBRAL HYPEREMIA 

Active or arterial hyperemia accompanies all the acute inflamma- 
tory affections of the brain, or may result from increase in blood 
pressure from any cause. Passive hyperemia results from any obstruc- 



532 DISEASES OF THE BRAIN AND MENINGES 



tion or impairment of the return flow, such as occurs from cardiac dila- 
tation, emphysema, asthma, or the pressure of tumors. 

There is no uniformity in the symptoms produced by hyperemia of 
the brain. Headache, restlessness, insomnia, delirium, mental dulness 
and coma have been attributed to this condition. It is difficult to 
separate the symptoms due to cerebral hyperemia from those produced 
by attendant conditions. 

CEREBRAL EDEMA 

Edema of the brain may accompany passive hyperemia and be due 
to the same cause. It may be part of a general anasarca, especially 
that of chronic Bright 's disease. It occurs in many local lesions of the 
brain, such as atrophy of the convolutions, thrombosis of the sinuses, 
tumors, or abscesses. 

In chronic alcoholism, a marked edema of the brain may develop, 
giving rise to the so-called wet brain. As in hyperemia it is difficult 
to separate the symptoms of edema of the brain from those of the 
underlying condition. (See Alcoholism, page 298.) 

CEREBRAL HEMORRHAGE, EMBOLISM AND THROMBOSIS 

Etiology of Hemorrhage. — Two factors are usually concerned: 
(1) An arteriosclerosis affecting the cerebral vessels and producing 
miliary aneurisms weakening their walls. Such a process may occur 
independently of general arteriosclerosis. (2) An increase in pressure 
in the vessels. 

The arteriosclerosis may depend upon any of the usual factors (see 
page 229). Emphasis should be placed on age, for cerebral apoplexy 
rarely occurs before 40, and increases in frequency mth advancing 
years. During parturition hemorrhage may be caused in the fetal 
head. 

High pressure may be caused by the same factors as the arterio- 
sclerosis. Chronic Bright 's disease is of especial importance, causing 
both arteriosclerosis and high blood pressure. 

Sudden increase in blood pressure due to anger, excitement, severe 
physical exertion, involving holding the breath and straining, the 
paroxysms of whooping-cough, or straining at stool may be the final 
determining cause of hemorrhage. 

Morbid Anatomy of Hemorrhage. — Hemorrhage may occur from 
any vessel, but is commonly from some branch of the middle cerebral 
artery. Hemorrhage may be minute or may destroy most of a hemi- 
sphere. More or less extensive laceration of the brain occurs, and fol- 
lowing this damage and the pressure of the hemorrhage, more or less 
extensive softening and necrosis of the brain substance. The necrosed 
tissue becomes yellowish or brownish and diffluent. Hemorrhages not 
infrequently break into the ventricles, filling them, and the blood may 
extend down the cord and be obtained by lumbar puncture. 



DISEASES OF THE MENINGES 



533 



Etiology of Thrombosis. — In thrombosis also there are two factors: 

(1) Disease of the vessel wall — arteriosclerosis. 

(2) Some changes in the blood favoring clotting, but of unknown 
nature. Whether thrombosis can occur from blood changes alone is an 
open question. Changes in the rate of flow may play a part, but these 
are ordinarily so slight as to render their influence doubtful. 

Thrombosis may be a complication or sequel of any of the acute 
infectious diseases — especially syphilis. In rare instances it occurs in 
youth, but is common from the twentieth to the fortieth year. 

Etiology of Embolism. — The usual origin of emboli is the heart, 
especially the lesions of the mitral valve, but emboli may come from 
the right side of the heart or any of the veins of the body, and 
passing through the wide pulmonary capillaries lodge in one of the 
cerebral vessels. Embolism may therefore occur at any period of life. 

Morbid Anatomy of Thrombosis and Embolism. — In either con- 
dition a clot, more or less extensive, is found in some vessel, usually a 
branch of the middle cerebral artery. In thrombosis there is local dis- 
ease of the artery wall — showing itself by atheroma, constriction, or dila- 
tation. In embolism the wall may be normal, though, of course, an 
embolus may lodge in a diseased vessel, if such be present. The first 
effect of an embolus or thrombus is to cut off the blood supply from the 
territory of the plugged vessel. An area of low pressure results 
into which blood must be crowded from the neighboring vessels, which 
in the cortex intercommunicate freely. Gradually, however, circula- 
tion is restored in the periphery of the area. The central part of it, 
being permanently shut off from the circulation, undergoes softening 
and necrosis. Such necrosis is likely to be extensive at the base of 
the brain, in the basal ganglia and internal capsule, where the arteries 
are terminal. Large areas of necrosis produce cysts full of bloody 
fluid; the smaller give rise to congested, soft, diffluent areas of less 
extent. 

Occurrence of Apoplexy. — Deaths from apoplexy constitute a con- 
siderable proportion of mortality statistics, about 1 in 22 of all deaths. 
Apoplexy is uncommon in childhood, common after 40 years, and in- 
creasingly frequent thereafter. 

Symptoms. Premonitory. — These depend upon preceding arterio- 
sclerosis, and include loss of mental activity, giddiness, insomnia, tem- 
porary aphasia or paralysis and the like. They are often entirely 
wanting. 

Apoplectic Attack. — Headache, vertigo, tingling or numbness in 
some part of the body initiate the disturbance. In at least one-half the 
cases stupor appears and increases to complete coma. With the coma 
the face is flushed, the respiration is rapid, deep, snoring, the pulse 
slow and full or rapid and weak. The tension is usually high, between 
200 and 300 mm., but may not be raised. The pupils are contracted 
or dilated, and often unequal. Conjugate deviation of the eyes is fre- 
quent, and the head may be turned toward the side of the lesion. The 



534 



DISEASES OP THE BRAIN AND MENINGES 



temperature is normal or subnormal at first, but rises to 101° to 103° P. 
in many cases, and may continue for some days (resorption of blood). 
All the muscles are relaxed, the reflexes usually abolished, and the 
sphincters incontinent. 

The characteristic paralysis now appears. Usually the whole of one 
side is involved. The cheek is puffed out in respiration, the arm and 
leg are flaccid, so that, if lifted, they fall like a dead weight. Unless 
the coma is profound, pricking the sound hand or foot will lead to vig- 
orous motion on the affected side no response is obtained. In some cases 
the affected side is rigid rather than flaccid. The paralysis may be 
limited to one arm or leg or one side of the face. 

Coma lasts a varying period and may persist till death, a week or 
more in some cases. Usually the coma passes off in a few hours (four). 
The deep reflexes return at the same time. The paralysis can then be 
better made out. On the paralyzed side the forehead cannot be 
wrinkled, the eye cannot be tightly closed, the face is flat from oblitera- 
tion of the naso-labial fold, the tongue protrudes toward the paralyzed 
side, neither hand nor foot can be raised or moved. Lesser degrees 
of paralysis both in extent and degree are of course seen. The palsy 
may be limited to one limb or to a single group of muscles. 

Course of the Affection. — In the worst cases the coma deepens, 
the disturbance of respiration and circulation becomes more profound, 
the respiration becoming irregular or Cheyne- Stokes, the pulse weak, 
irregular and intermittent, the blood pressure higher, and death ensues 
in the course of a few hours or after a week. In such cases fever is 
present and often mounts steadily toward the end, reaching in some 
instances 107° to 108° P. 

Recovery occurs in most cases. After return of consciousness the 
paralysis begins to show improvement. This may be almost immediate 
or may show itself only after some days. Return of power is first seen 
in the muscles about the eye, so that it is often said that upper branches 
of the facial nerve are not involved in cerebral paralysis. Power re- 
turns in the leg before the hand and in the shoulder, elbow, hip and 
knee, before wrist or ankle, although the first evidence of returning 
power is often seen in ability to move the fingers or toes. Recovery may 
be rapid and complete, so that in a few days or weeks power may be 
restored. Usually it is a matter of weeks or months, and some paraly- 
sis, commonly of the hand and arm or the face, is left. Ability to walk 
is nearly always recovered. The gait is characteristic on account of 
the inability to raise the toe; the foot must be swung outward and the 
toe dragged, and the sole brought down with a flap (drop-foot). If 
the paralysis persists rigidity develops in the paralyzed muscles and 
contractures, especially in the arm and hand. Later tremor and chorei- 
form or athetoid movements may develop. The reflexes on the 
paralyzed side become much exaggerated and continue so. The mus- 
cles may undergo some atrophy. 

Influence of Site of Lesion. — The description given applies to 



DISEASES OF THE MENINGES 



535 



lesions involving the motor tract, the usual site, but hemorrhage, em- 
bolism or thrombosis may involve other areas and give rise to special 
symptoms, combined with or independent of the hemiplegia. 

Aphasia is quite regularly produced by a lesion involving the left 
motor area in right-handed people or the right in the left-handed. It 
is usually recovered from, but with some permanent defect. Mental 
symptoms, confusion, inability to think or to remember, with lack of 
control and emotional excitement, may accompany hemiplegia and per- 
sist for some time. Hemianopsia of the bilateral homonymous type, 
that is involving the like-named (right or left) halves of both visual 
fields, results from lesions affecting the occipital lobes. 

Word-blindness may follow lesions of these lobes. Hemianesthesia 
may accompany hemiplegia, but is usually only partial and quickly 
disappears. Cerebellar symptoms, vertigo, staggering gait and double 
vision may follow a hemiplegic attack. In cortical lesions paralysis may 
be very limited. In lesions of the internal capsule paralysis is 
extensive. 

Lesions of one crus cause loss of ability to move the eye of the 
paralyzed side upward, downward or inward, the pupil is dilated and 
there is ptosis (third nerve). Lesions of the pons, if in its lower half, 
may cause paralysis of one side of the face and the opposite side of the 
body-crossed paralysis. In this condition the upper branch of the 
facial nerve is involved and the eye cannot be closed. 

Diagnosis. — The focal symptoms, hemiplegia, etc., are of prime 
importance. If the patient is conscious, he will call attention to the 
loss of power, which in such cases may be limited to one extremity, or 
to the face. The absence of any local signs, pains or tenderness of nerve- 
trunks, the normal electrical reactions, as well as the sudden onset, 
exclude neuritis, and indicate a paralysis of central origin. 

Whether such paralysis is due to definite organic lesion, such as 
hemorrhage, embolism or thrombosis, or is caused by the so-called func- 
tional disturbances, spasm of the cerebral vessels, or localized edema 
or anemia of the brain cannot be at once determined. The functional 
palsy will disappear in a few hours ; an apoplectic lesion will cause par- 
alysis lasting several days. 

Apoplexy with coma is distinguished by the depth of the coma (the 
patient cannot be roused), the paralysis, the flaccidity or rigidity of 
the affected side, inequality of the pupils, and absence of reflexes. 

Opium poisoning, alcoholism, uremic coma must be excluded. The 
pin point pupils and slow respiration mark opium or morphine poison- 
ing. Alcoholic coma is less profound; the patient can be roused by 
pressing on the supraorbital nerves or by the policeman's method of 
beating the soles of the shoes with his night-stick; the speech is thick 
and incoherent; there is no paralysis; the pulse is rapid, full and 
bounding, the breath is strongly alcoholic and the stomach contents 
consist of food and alcoholic beverages. Uremic coma is more difficult 
to distinguish, especially as it may be accompanied by temporary paraly- 



536 DISEASES OF THE BRAIN AND MENINGES 



sis. Edema, anemia, the urinous odor of the breath, the history, if ob- 
tainable, may point to nephritis. The urine will usually be scanty, 
contain much albumin, many casts, and possibly blood. There is no 
inequality of the pupils, no deviation of the eyes, and paralysis, if 
present, is limited and partial. 

Differentiation between Hemorrhage, Embolism and Throm- 
bosis. 

Embolism occurs at any age, the onset is sudden without coma, the 
paralysis usually extensive at first clears rapidly, the pupils are un- 
affected, the pulse that of heart disease, the respiration normal. The 
presence of a definite valvular lesion, especially of the mitral, is the 
most convincing point. 

Between hemorrhage and thrombosis, distinction is difficult and at 
best uncertain. 

Thrombosis^ however, belongs particularly to the syphilitic, with 
preceding symptoms of cerebral arteriosclerosis. Apoplexy in men 
below the age of 40 is very likely to have this origin. The onset is 
sloAver than in hemorrhage. The coma is not so deep, the pupils are 
unafi:ected, the pulse does not become slow, and the respiration is not so 
much affected (there is no increase of intracranial pressure). The local 
symptoms are not so extensive as in hemorrhage, and improve consid- 
erably in the first few days. 

Prognosis. — Apoplexy is always grave. Complete recovery from a 
first attack is possible, but recurrence is almost sure to follow and 
attacks may be repeated for years. The patient may, however, enjoy 
comparative comfort in the intervals. The older the patient, the more 
extensive the paralysis, the deeper the coma, the graver the prognosis 
becomes. 

Treatment. — The patient is put to bed, the head elevated. If the 
blood pressure is high, the face congested, the pulse strong, venesection 
Is indicated. From 12 to 16 ounces of blood may be dra^^^i. Nitro- 
glycerine may be used for the same purpose, 1/100 gr. every hour or 
half hour till the tension is relieved. The bowels may be freely moved 
by two drops of Croton oil mixed ^vith butter and dropped far back 
on the tongue. Absolute quiet and careful nursing are imperative. 
Care should be taken to secure unembarrassed breathing and to prevent 
the inhalation of food materials or the secretions of the mouth and 
throat. No effort to feed need, as a rule, be made till the patient can 
swallow, but food or water may be given by gavage, if necessaiy. 

For retention of urine catheterization may be required. 

In convalescence passive motion of the affected parts, with rub- 
bing and manipulation, should be employed to maintain the muscular 
tone and prevent contractures. Electricity may be used for the same 
purpose. The patient is to be encouraged to exercise every muscle as 
he can. 

In embolism or thrombosis, if the diagnosis is sure, the head should 
be kept low and stimulants administered, such as nitroglycerine, caffeine 



CEREBRAL PARALYSIS OF CHILDHOOD 537 



or strychnine. If the diagnosis is uncertain these measures should not 
be ventured. The general measures applied to hemorrhage should then 
be followed. 

CEREBRAL PARALYSIS OF CHILDHOOD 
(Infantile Hemiplegia or Diplegia. Infantile Paralysis) 

Definition. — Loss of either motion or sensation, or both, due to brain 
lesion. In children these conditions are frequently accompanied by 
defective mentality, many of the patients being imbeciles or idiots. 

Etiology. — Many of these cases are traumatic, the results of cere- 
bral hemorrhage at birth, due to protracted labor or instrumental in- 
terference. Some of them depend on an arrested development of the 
brain caused by a preceding lesion of some of the cerebral vessels, em- 
bolism, rupture, or thrombosis. Some are due to inherited syphilis. 
Not infrequently no satisfactory causation can be given. 

Pathology. — The brain lesions underlying these paralyses are varied, 
including: 1. Atrophy of some greater or less part of the brain cor- 
tex due to preceding vascular lesion. The convolutions are small, the 
affected part, usually that supplied by the middle cerebral artery, is 
shrunken. Over the atrophic area there is a collection of fluid or the 
overlying membranes are thickened. 

2. Porencephalus, a condition marked by the formation of holes or 
cavities in the brain. If such holes or cavities contain fluid they con- 
stitute cysts. 

3. Maldevelopment. An undeveloped condition of the brain, the 
ceUs resembling those of the new-born, without other gross lesion. 

4. Hydrocephalus — either external or internal, (a) External hydro- 
cephalus, the collection of excessive fluid on the surface of the brain, a 
very rare condition. It doubtless results from meningitis or atrophy, 
the fluid in the latter case being poured out to fill the empty space, 
(b) Internal hydrocephalus, an unusual accumulation of fluid in the 
ventricles clue to obstruction in the iter or the fourth ventricle (foramen 
Magendie), preventing the normal flow of fluid from the lateral ventri- 
cles to the subdural space. With hydrocephalus the ventricles are dis- 
tended, the cortex thinned, until only a thin sac remains. In hydro- 
cephalus the head is large ; it may be enormous. The f ontanelles are 
abnormally long in closing, or remain open. The measurements are 
increased in all diameters. In the other conditions described the head 
is small (microcephalus) and often asymmetrical. 

Symptoms. — Onset. These patients are rarely seen at the onset 
of the primary trouble, hemorrhage, embolism or thrombosis, which 
most often underlies the permanent affection, but are brought to the 
physician for the paralysis or mental condition. If the condition pre- 
cedes birth, the onset is not observed and only the sequelae or per- 
manent conditions are noted. At birth cerebral hemorrhage causes 
difficulty in making the child breathe, or cry, cyanosis, possibly convul- 
sions, and often death. 



538 



DISEASES OF THE BRAIN AND MENINGES 



After birth, paralysis most often follows one of the acute infec- 
tious diseases, measles, scarlet fever, influenza, etc., and is ushered in 
by convulsions, fever, vomiting and stupor. The paralysis is noticed at 
once and runs the course of apoplexy in later life. Later symptoms or 
sequelae include: (1) Motor defects, (2) sensory defects, (3) mental 
defects. 

(1) Motor defects. Usually on one side, sometimes on both, we 
find the conditions characteristic of hemiplegia, loss of power, spas- 
ticity, contractures and exaggerated reflexes. The loss of power is par- 
tial only. The patient can walk, but with the characteristic gait ; and 
may be able to use the hand, but awkwardly. Spasticity is most marked 
in the legs, and if both are affected (paraplegia) the knees overlap in 
walking. Contractures are most marked in the upper extremity, both 
elbow and wrist being flexed and incapable of extension. Rarely there 
is no spasticity, and no increase in reflexes. 

(2) Sensory defects include blindness, hemianopsia, deafness, rarely 
loss of smell or taste. 

(3) The mental defects are of all grades. The idiots are incapable 
of grasping new ideas and cannot be taught to keep themselves clean. 
The imbecile can be taught cleanliness and grasps simple ideas, may 
learn to recognize persons and to speak a few words, but is far below 
normal standards of mentality. 

Associated disturbances. (1) In the paralytic limbs athetoid or 
choreiform movements may occur. The latter simulates the quick, jerky 
movements characteristic of chorea. Athetoid movements are slower, 
more rhythmical, flexions and extensions, or rotations of joints, such 
as those of the fingers or wrist. These may occur only upon attempts 
to use the limb or may be constant. (2) Epilepsy is a common accom- 
paniment; the attacks may be general, or of the Jacksonian type. (3) 
Aphasia is common in those suffering from right hemiplegia. 

Prognosis. — This is always unfavorable. The lesions and the result- 
ant failure of brain development are permanent. 

Treatment. — For apoplexy in a child the same general measures as 
apply in adults are to be used. For the after-results, the paralysis and 
mental defects, in the severer grades nothing can be done. In the milder 
grades special education in institutions or under trained teachers may 
bring improvement. Massage and passive motions of the paralyzed 
limbs may be helpful. 

Double spastic paraplegia (Little's disease) has in some cases been 
benefited by cutting the posterior nerve-roots belonging to the affected 
parts. 

Operations upon the heads of these children for the relief of an 
assumed pressure due to microcephaly or for the drainage of cysts have 
proven fruitless. 

Hydrocephalus. — If this precedes birth the large head may be an 
obstacle to delivery, sometimes re(]uiring the sacrifice of the child. 
Often the child appears normal at birth; the enlargement of the head 



ABSCESS OF THE BRAIN 



539 



and failure of the child to develop first attracting attention about the 
sixth month. The size of the head and the failure to develop mentally 
are first noted. The fontanelles remain open and fluctuate. The size 
of the head increases steadily. Nystagmus, strabismus and blindness 
from optic atrophy are common. Muscular weakness is marked, so that 
the child cannot sit or stand, and may not be able to raise the head. A 
spastic condition in all four extremities with atrophy from disuse is 
common. Vomiting is frequent. Convulsions occur from time to time. 
In these severe cases the child never learns to walk or talk and usually 
dies within the first year or two. In the milder grades the child grows 
and develops mentally. A slight hydrocephalus is not inconsistent 
with full mental ability. Between these limits there are many cases in 
which great enlargement of the head is associated with defective power 
in one or both sides of the body and imperfect mental development. 

ABSCESS OF THE BRAIN 

Etiology. — Abscess of the brain results from the lodgment of pyo- 
genic micro-organisms. These secure admission either (1) directly from 
some local focus — otitis media, either acute or chronic, suppuration of 
frontal or ethmoidal sinuses or of the orbit, from penetrating and in- 
fected wounds of the skull or operations — or (2) indirectly through the 
blood stream, in pyemia, malignant endocarditis, septicemia, pneumonia 
and the like conditions in which pyogenic cocci are found in the blood. 
The second group is of lesser importance because the conditions are 
practically always fatal. In the first group of cases there is hope of 
prevention or adequate treatment. 

Morbid Anatomy. — The abscesses may be single or multiple. The 
pyemic abscesses are usually multiple. The single abscess most often 
results from local infection. The abscess is large or small, and may 
occur in any part, but is most frequent in the temporo-sphenoidal lobe, 
because of its relation to the ear. The pus is usually greenish and foul. 
Any of the pyogenic cocci may be found in it. A suppurative menin- 
gitis, either local or general, commonly accompanies the abscess. 

Symptoms. — These are notoriously vague and unsatisfactory. The 
rational symptoms of suppuration, chills, fever, sweating, anemia and 
emaciation, may be present, but are rarely observed unless from the 
primary process. Fever is ordinarily slight, may show remarkable 
fluctuations, is often absent. A leukocytosis is quite constant, and the 
differential count may show an increase of the polynuclear cells. 

The cerebral symptoms are those of increasing intracranial pressure 
and an abscess in this respect closely resembles a tumor of the brain. 
Headache is common, severe and persistent. Vomiting may occur quite 
regularly. The pulse is often slow, respiration slow and irregular. The 
pupils may be dilated or unequal. Optic neuritis (choked disc) may 
develop, but is often wanting. The mental state is one of indifference 
or stupor; convulsions may occur. 

Focal symptoms. Muscular rigidity or paralysis, aphasia and sen- 



540 



DISEASES OF THE BRAIN AND MENINGES 



sory disturbances, if the proper areas of the brain are involved, may be 
present, but are often lacking, especially in abscesses secondary to otitis 
media. 

Ocular symptoms, such as inequality of the pupils, conjugate devia- 
tion or strabismus, or paralysis of one or more muscles, may be observed. 

The COURSE of abscess of the brain is as variable as its symptoma- 
tology. The cases may be grouped as follows: (1) Latent. The 
abscess for months or even years gives few symptoms, a little headache, 
an occasional rise of temperature, 'mild prostration, and is not recog- 
nized till a terminal suppurative meningitis or the autopsy reveals the 
condition. (2) Tumor-like. The symptoms are slowly evolved and 
suggest tumor of the brain. (3) Fulminant. The course may be very 
short and sharp, the symptoms closely reproducing the picture of acute 
suppurative meningitis. 

The termination is usually marked by the extension of the inflamma- 
tion to the pia mater of the brain and cord, a suppurative meningitis. 

Diagnosis. — The most important point is the cause. Obscure or 
severe cerebral symptoms following otitis media, acute or chronic, a frac- 
ture of the skull, etc., should always cause suspicion of the presence of 
an abscess. 

Signs of cerebral irritation, persistent headache, vomiting, stupor, 
convulsions or coma, without meningitis — slight rigidity of the neck, 
no Kernig's sign, no Babinski reflex, clear cerebrospinal fluid, espe- 
cially if accompanied by fever, and leukocytosis are important. 

Focal symptoms, paralysis, aphasia, deafness on one side, hemianop- 
sia, are only rarely present. Tenderness of the skull to pressure or 
percussion immediately over the abscess is unusual. The localization 
must be made in most cases from the cause. If from ear disease, the 
abscess is looked for in the temporo-sphenoidal lobe; if from a nasal 
condition, in the frontal lobe ; if from a fracture, in relation to the 
bone lesion. 

Prognosis. — The outlook is always grave. Formerly always fatal, 
about 50 per cent, of the patients are now saved by proper surgical 
treatment. 

Treatment. — Prophylaxis is most important. The aseptic or anti- 
septic management of fractures of the skull, suppurations of the ear, 
and other possible sources of cerebral abscess is essential. When an 
abscess has formed, trephining and drainage are essential. 

GENERAL PARESIS 
(Dementia Paralytica. Progressive Paralysis of the Insane) 

Definition. — A chronic progressive disease of the brain and cord, 
marked by motor and psychical disturbances and ending in complete 
paralysis and dementia. 

Etiology. — General paresis is a disease of adult life, affecting men 
much more often than w^omen, due to the strain of modern life, and, 



GENERAL PARESIS 



541 



in most cases, the remote effects of syphilis. Syphilis is held to be the 
basis of the disease, and for this reason the disease frequently presents 
itself in both hnsband and wife. Prom five to twenty-five years may 
intervene between the initial lesion and the development of symptoms 
of paresis. Excess of any kind, hard work, w^orry, over-indulgence in 
alcohol, are secondary factors in causing the disease. General paralysis 
is very closely related to locomotor ataxia. 

Morbid Anatomy. — Changes are found both in brain and cord. In 
the brain pachymeningitis, with thickening and cloudiness of the pia 
mater and adhesions between the two membranes, is common. With 
these changes atrophy of the cerebral cortex, particularly the frontal 
and parietal lobes, shown by thinning of the convolutions and deepen- 
ing of the gyri and diminished weight of the brain, is combined. 

Arteriosclerotic changes in the cerebral vessels constitute the 
third important feature. Hydrocephalus, both internal and external, 
is common. 

Microscopically the changes in the vessels and inflammatory infil- 
tration of the pia and dura are associated with degenerative changes in 
the cortex, especially of the ganglion cells. Many of these disappear, 
those remaining show marked degeneration. The neuroglia fibers, the 
spindle cells and nuclei of the neuroglia are increased. 

The changes of general paresis are not limited strictly to the frontal 
and parietal regions, but are found to some extent in other parts, even 
in the cerebellum and pons. 

Symptoms. — The onset of paretic dementia is peculiarly insidious 
and gradual. The symptoms are both mental and physical. Often the 
initial symptoms are neurasthenia, mental depression, headache, sleep- 
lessness, dizziness, fatigue. 

Defects of judgment then appear. A man becomes careless in his 
habits, neglectful of his person, of his business, of his relations to his 
family and others. Petty thefts may be committed, checks signed heed- 
lessly, those about him subjected to evidences of irritability or anger 
without reason. In some cases an exaggerated love of showy dress, or 
extravagance in expenditure, or excessive sexual indulgence marks the 
loss of self-control. Defects of memory become marked. The patient's 
age, or address, or the names of well-known persons or places are for- 
gotten. He becomes unable to spell or to do simple sums in arithmetic. 
Things brought to his attention are immediately forgotten, until the 
mind becomes a complete blank. Delusions of grandeur are not uncom- 
mon, the patient imagining himself to have become enormously rich, 
or powerful, or to be engaged in large undertakings. Melancholic or 
depressive delusions occur in some cases, but are unusual. In all cases 
there is a progressive apathy or indifference to surroundings and to his 
own mental state. Convulsions or apoplectic attacks are common. The 
convulsions may be general or of the localized Jacksonian type. The 
attacks of paralj^sis are transitory, either hemiplegia or aphasia. In 
fatal cases no sufficient cause for the paralysis can be found. 



542 



DISEASES OF THE BRAIN AND MENINGES 



The PHYSICAL SIGNS are striking. (1) Eye phenomena. Reflex 
immobility of the pupil. Reaction to light alone may be lost (Argyll- 
Robertson pupil) or to both light and accommodation. The pupils may 
be unequal, or irregular, or paralyses of ocular muscles may develop. 

(2) Facial signs, (a) Disturbances of speech are among the earliest 
and most important symptoms. The patients have difficulty in pro- 
nouncing consonants, particularly 1 and r, and the defective memory 
shows itself strikingly in inability to repeat simple series of words joined 
by sound rather than by sense, such as "truly rural," "third artillery 
brigade," or "round the rough and ragged rock the ragged rascal ran."^ 
(b) Tremors of the facial muscles and the tongue are commonly present. 

(3) Ataxia. Muscular movements of any kind are awkward and asso- 
ciated with tremor. The writing shows this particularly well. The 
letters show the tremor of the hand, the words are written in any direc- 
tion and letters or syllables are omitted. (4) The deep reflexes are 
lost or exaggerated, especially the Achilles and patellar reflexes. (5) 
Muscular weakness is pronounced, especially late in the disease, when 
the patients are bedridden; in consequence atrophy results from disuse. 
(6) Trophic disturbances occur late in the disease. Bed sores, perfor- 
ating ulcers of the foot, or gangrene of an extremity may develop. (7) 
The blood gives a Wassermann reaction in 75% to 80% of cases. The 
cerebrospinal fluid regularly shows an unusually large number of hTuph- 
ocytes. 

Course. — The disease is progressive and ends in dementia. The 
duration is usually several years — from 2 to 15 or 20. In the end the 
patient becomes bed-ridden, devoid of intelligence, and loses power over 
the sphincters, so that the urine is retained or passed involuntarily, and 
the feces are passed unconsciously. He dies of exhaustion or of inter- 
current disease, such as cystitis or septicemia. 

Prognosis. — Recovery is possible but exceedingly rare. Remissions 
may occur, lasting for years. 

Diagnosis. — Typical cases can hardly be mistaken. In the early 
stages the disease may be confused With neurasthenia. The combina- 
tion of mental symptoms with the definite physical signs of paresis 
should distinguish it. The Wassermann reaction and examination of the 
cerebrospinal fluid are helpful. Disseminated sclerosis, especially in 
its terminal states, may be confused with paresis. The mental condi- 
tion should be sufficient to make the distinction. Cerebral syphilis is 
distinguished with difficulty, because the diseases are closely related and 
cerebral syphilis may terminate in general paresis. The course of the 
disease under treatment is the surest guide. Cerebral syphilis will im- 
prove more promptly and decisively than will paresis. 

Alcoholic dementia is marked by a history of alcoholism, the physi- 
cal evidences of chronic alcoholism, possibly peripheral neuritis, an 
absence of the pupillary signs, and by characteristic hallucinations and 
delusions. 

Treatment. — Vigorous antisyphilitic treatment, salvarsan followed 



MULTIPLE SCLEROSIS 



543 



by mercury by injection or inunction and increasing doses of potassium 
iodide, up to 30 or 60 grains thrice daily, should be tried in specific 
cases. The Wassermann reaction may be followed, but should not con- 
trol the treatment. 

Complete mental rest, careful feeding and judicious supervision, 
such as can ordinarily be obtained only in a sanatorium, are indicated 
in all cases. The bromides or chloral may be used for epileptic seizures or 
convulsions. Hydrotherapy and massage are helpful in the early stages. 

MULTIPLE SCLEROSIS 
(Disseminated Sclerosis; Insular Sclerosis) 

Definition. — A chronic affection of the brain and cord, due to re- 
placement of scattered areas of nerve-cells or nerve-fibers by fibrous tissue. 

Sclerosis of the central nervous system occurs under a great variety 
of conditions, in which the fibrous tissue appears as a replacement 
process, designed to fill the gap left by destruction or degeneration of 
the nerve tissue, or as a terminal step in an inflammatory process. 
Sclerosis regularly includes thickening of the pia arachnoid and in- 
crease in the neuroglia tissue of the cerebrospinal axis; Thus it is seen 
in more or less extensive areas of the brain following vascular lesions, 
as in the cerebral palsies of childhood or in tabes dorsalis, lateral 
sclerosis, the ascending and descending degenerations, following trans- 
verse lesions of the cord, or following meningitis or other inflammatory 
lesions. 

But independently of all such conditions sclerosis occurs in isolated 
or disseminated areas of the brain and cord as an independent affection. 

Etiology. — The disease occurs frequently at all ages in either sex. 
Many causative factors have been advanced, such as syphilis, or other 
acute infectious disease, exposure to cold and wet, and the like ; none of 
them is sufficiently constant to be important. 

Morbid Anatomy. — The essential feature is areas of fibrosis of the 
brain and cord scattered at haphazard throughout them. The brain or 
cord may show areas of atrophy corresponding to the sclerosis. Opaque 
patches in the pia mater may overlie the placques of fibrous tissue, and 
the affected areas may be firmer than normal. On section these areas 
are found to be gray or grayish red foci of connective tissue. ]\Iicro- 
scopically an increase of fibrous tissue with disappearance of nerve- 
cells and nerve-fibers in the affected part of the cord or brain is found. 

Symptoms. — As these must depend upon the location and order 
of development of the sclerotic foci in the brain and cord the clinical 
picture necessarily varies greatly, the characteristic feature being that 
the symptoms present evidences of involvement of various areas of the 
brain and cord independent both in time and position of one another. 
In most cases the following symptoms are noted : 

1. Spinal, (a) Paraplegia, usually of spastic type. IMore or less 
difficulty in walking develops, possibly with spasticity, and overlapping 
of the knees as the feet are advanced, (b) Intention tremor, usually 



544 



DISEASES OF THE BEAIN AND MENINGES 



most marked in the hands, but also in the legs, or in neck and face. 
The tremor is rapid, from 4 to 7 per second, and varies in degree, so 
that it may be slight or so severe as to render such acts as drinking 
water almost impossible. This tremor appears only on effort; at rest 
the muscles are quiet. Charcot's explanation that the tremor results 
from difficulty in the transmission of motor impulses through sclerosed 
areas seems to best fit the case, (c) Difficulties in micturition and defe- 
cation may appear early, and are regularly present late. Delay in start- 
ing the urine, retention, or incontinence may develop. Constipation is 
the rule ; fecal incontinence develops in the final stages, (d) Sensory dis- 
turbances, tingling, numbness, shooting pains, formication and the like 
may aff'ect either upper or lower extremities, (e) Reflexes. The ten- 
don reflexes are exaggerated. The abdominal skin reflex is absent. 
Babinski's reflex is present. 

2. Cerebral, (a) Scanning speech. The speech is slow and meas- 
ured, the voice monotonous. In the later stages each word or even 
syllable must be pronounced slowly and with effort. The difficulty in 
speech may be associated with tremor of the facial muscles, (b) Ocu- 
lar symptoms. Diplopia from partial or complete paralysis of ocular 
muscles, nystagmus on movement of the eyes, or even at rest, or in- 
equalities of the pupils may be present. The nystagmus is very char- 
acteristic. Blindness may result from optic atrophy, (c) Vertigo or 
vomiting may occur, (d) Mental debility, shown by impairment of 
memory, false hopefulness or undue depression, or lack of emotional 
control, may be shown. 

Course and Prognosis. — The course of the disease varies remark- 
ably. Remissions lasting years occur and symptoms come and go. 
Even optic atrophy has been recovered from. As a rule the disease is 
progressive and incurable, yet the patients live for years. 

Diagnosis. — From hysteria, multiple sclerosis is distinguished by the 
ocular symptoms, especially nystagmus or optic atrophy, the intention 
tremor, disturbances of the bladder, the Babinski reflex. General pare- 
sis presents earlier mental disturbances with a history of syphilis, the 
Argyll-Robertson pupil, diminished or lost knee-jerks, the presence of a 
lymphocytosis of the spinal fluid, without nystagmus, intention tremor 
or the scanning speech. Paralysis agitans is marked by tremor which 
is constant, not intentional, and without nystagmus, scanning speech, 
exaggerated reflexes, or Babinski's sign. 

Treatment. — Life in a mild climate, freedom from labor or anxiety, 
a nutritious diet and exercise carefully regulated to prevent fatigue 
are to be enjoined. Medicines cannot affect the underlying process. 
Constipation and other symptoms are to be treated as they arise. 

TUMORS AND CYSTS OF THE BRAIN 
Etiology. — Brain tumors occur at all ages, in men more often than 
women. A preccnling tuberculous or syphilitic affection may be of im- 
port, otherwise the etiology is not known. 



TUMORS AND CYSTS OF THE BRAIN 



545 



Morbid Anatomy. — Many varieties of brain tumor are known — 
the common ones are tubercle, sarcoma, glioma, gumma and carcinoma. 
Tubercle occurs in the form of large, isolated and usually single tumors 
made up of masses of miliary tubercles or a single large tubercle as 
much as an inch or an inch and a half in diameter. Tubercle in the 
form of tumor is common in childhood, rare in later life. Gumma, on 
the other hand, never results from inherited syphilis, and is therefore 
very rare in childhood, but common in adult life. Sarcoma or car- 
cinoma may follow a primary growth elsewhere, but is usually primary 
in the brain. Glioma is a growth of neuroglia, and therefore peculiar 
to the nervous system. Cystic tumors of the brain may arise from 
parasitic infections, such as echinococcus or cysticercus. They are very 
uncommon in this country. Fibroma, angioma, myxoma, osteoma and 
other rare forms are known. 

In brain tumor the intracranial pressure is always increased, and 
if the skull is opened during life the dura bulges and its pulsation is 
diminished. The cerebral convolutions are regularly flattened. The 
ventricles often contain excess of fluid owing to obstruction of the ven^e 
Galeni by pressure. 

Symptoms. — These are both general and focal. 

General. — These are produced by the steadily increasing intra- 
cranial pressure. (1) Severe and persistent headache. (2) Mental 
disturbance. The disposition may change notably, and the patient be- 
come irritable, careless or indifferent. Memory is impaired and atten- 
tion fails. The patient may become dirty and untidy in his habits. 
(3) Vertigo and vomiting. Dizziness is common in any cerebral tumor, 
but is pronounced if the cerebellum is involved. Vomiting is frequent, 
and is usually projectile in type. (4) Slow pulse. The rate is slow, 
50 to 60, the pulse full and of high tension. (5) Convulsions. These 
may be general or of the Jacksonian type. (6) Choked disk is present 
in 80 to 90% of brain tumors, and constitutes one of the most important 
signs of brain tumor. Amblyopia, defective vision or blindness may 
accompany the choked disk. The field of vision may be contracted with 
inversion of the color-fields, so that the field for blue may interlace with 
or lie within that for red. 

Focal Symptoms. — These depend upon the location. 

Frontal Region. — Changes in temperament and mental activity are 
notable. Memory is impaired, ability to concentrate thought or to learn 
diminishes, and the patient becomes stupid and irritable, or uncon- 
trollable. 

Tumors of the third left frontal convolution in right-handed per- 
sons cause motor aphasia with agraphia. In left-handed persons the 
tumor must be in the right hemisphere. 

Motor Area. — Tonic or clonic spasms of the muscles of some por- 
tion of the body are caused by tumors of the motor cortex. The 
spasms so caused occur at intervals and may terminate in general con- 
vulsions. The spasms always begin in those muscles whose centers of 
35 



546 



DISEASES OF THE BRAIN AND MENINGES 



representation are most affected by the tumor. Therefore, observation 
of these spasms as to their location at the beginning and the mode of 
spreading helps greatly in locating a tumor. Either extremity or the 
face may be affected. Paralysis or paresis may follow either in arm, 
leg or face, but cortical tumors rarely produce hemiplegia. Tumors 
involving the internal capsule or the motor tract beyond it may cause 
hemiplegia. 

Parietal Region. — Disturbances are not constant, but in many cases 
impairment of sensation or muscular sense follows. Word-blindness 
has been found to be due to lesion of the inferior parietal lobule (left). 

Occipital Region. — Hemianopsia (bilateral homonymous) results 
from lesion of the occipital lobe. It may be unknown to the patient 
and must be tested for. 

Island of Reil. — Tumors of this area produce paraphasia — that is, 
disturbance of speech in which one word is regularly substituted for 
another. They may produce pressure upon the neighboring face cen- 
ters or even upon the internal capsule. 

Crus. — Tumor involving the crus should produce paralysis of the 
third nerve of the same side and the extremities of the opposite side of 
the body. The fourth nerve may also be involved. 

Pons. — Tumors in the upper part involve the third and fifth, in the 
lower part, the fifth, sixth, seventh and eighth. In this situation par- 
alysis of one or more of these nerves with loss of power on the opposite 
side of the body, so-called alternating hemiplegia, may result. 

Medulla. — The ninth, tenth, eleventh and twelfth nerves suffer with 
resulting difficulties in swallowing, in respiration, irregularity of the 
pulse, and paralysis of the tongue. Polyuria or glycosuria may also result. 

Cerebellum. — Because of the small space in which the cerebellum 
lies enclosed by the tentorium cerebelli, small tumors produce severe 
results. By compressing the fourth ventricle, tumors in this region 
cause distention of the ventricles above, and hence sj^mptoms appear 
early. Staggering gait, vertigo and cerebellar ataxia, an incoordination 
which entirely disappears when the patient lies down, are marked. 
Nystagmus is frequently present. Knee-jerks are exaggerated. 

Diagnosis. — The symptoms of steadily increasing intracranial 
pressure with the presence of choked disk are characteristic. Abscess 
of the brain must be excluded by the absence of any cause for suppura- 
tion, absence of any constant leukocytosis, or fever, or other con- 
stitutional symptoms of suppuration and the presence of optic neuritis. 
Brain abscess rarely gives rise to definite focal symptoms and then only 
late in the disease. 

Tubercular meningitis causes a more rapid development of symptoms, 
with hyperesthesia to light or sound, possibly tubercles in the chorioid, 
and without optic neuritis. Tubercle bacilli should be found in the 
spinal fluid. Chronic hydrocephalus in children is excluded by the size 
and shape of the head, the symmetry of the rigidity or loss of power^ 
absence of choked disk, and the comparative comfort of the patients. 



APHASIA 



547 



The Wassermann reaction is a valuable aid in the diagnosis of 
gumma. 

Course and Prognosis. — Gradual but steady increase in symptoms 
over one or two years is the usual history. Death at the end of two 
or three years results in nearly all cases. Gummata may be relieved, 
possibly cured by specific treatment. A few tumors have been success- 
fully removed by surgery, but only ten per cent, are operable, and of 
those operated upon but few survive. 

Treatment. — Active antisyphilitic treatment should be tried. The 
iodide of potassium is given in increasing doses up to 60 grains thrice 
daily. Inunctions of mercurial ointment or injections of mercury may 
be combined with the iodide. Careful study should be made in the 
effort to locate the tumor and operation undertaken, if it is accessible. 

APHASIA 

Definition. — Literally the word means loss of the power of speech, 
but in medicine includes all the disturbances of the use of language, 
either written or spoken, not dependent on intellectual failure or par- 
alysis of the vocal organs. Aphasia is a symptom of various cerebral 
lesions, not a disease in itself. The exact determination of the defect in 
speech is of material aid in the location of cerebral lesions, especially 
brain tumors. The subject is, therefore, of sufficient importance to be 
dealt with separately. 

To understand the different types of aphasia one must go back to 
the mental processes underlying the use of words in speaking or writ- 
ing. Every word has four points of relation or centers in the cerebral 
cortex. It can be heard or seen, it may be spoken or written. Thus 
the auditory center lies in the temporal lobe, the visual center in the 
angular gyrus, the motor speech center in the third left frontal con- 
volution, and the center for writing in close relation to it in the centers 
for arm and hand. Each of these actions depends upon the integrity 
of a definite area of the cortex, and also the normal use of words in 
speaking and writing depends not only upon integrity of these centers, 
but on their free communication with one another through the associa- 
tion fibers of the brain. 

The chief types of aphasia are described thus : 

1. Sensory Aphasia.— 1. Word-Deafness. — This condition is best 
illustrated by the common experience of forgetting names. Every one 
has at some time seen an acquaintance whom he sees, recognizes, per- 
haps knows all about, and yet cannot name. The memory picture of 
his name cannot be recalled and hence cannot be expressed. But if 
now the acquaintance says my name is John King, the recollection may 
still fail, if the defect is complete, but usually the sound of the 
name at once recalls its word picture and one recognizes its propriety 
and utters it. The condition here described is, of course, a matter of 
momentary forgetfulness, but in true word-deafness the condition 
persists. The patient is therefore unable to name familiar objects when 



548 



DISEASES OF THE BEAIN AND MENINGES 



brought to mind in any manner. In this condition there must be a 
cortical lesion involving the sound memory centers in the temporo- 
sphenoidal lobe. If the defect is but partial, the name of a thing can- 
not be recalled of one's self, but is recognized at once when heard. 
This auditory amnesia, as it is sometimes called, implies the integrity 
of the word-centers, but a defect, sub-cortical, in the fibers connecting 
them with other centers. This distinction between cortical and sub- 
cortical lesions is of importance mainly with reference to the possibil- 
ity of operating upon cerebral lesions such as tumors. 

2. Word-Blindness. — If this condition is complete word pictures are 
entirely lost. The thing seen is not recognized, and hence cannot be 
named. If the defect is partial only, the missing word picture, not 
reached by one route, the eye for example, can at once be recalled if 
the approach is made through another channel such as the ear. Thus 
a patient with complete word-blindness cannot recognize and name a 
bell, for example, when seen, but if it is rung in his ear he recognizes 
it at once and on request draws it in outline. He has the concept of a 
bell with its form, but it cannot be reached through the visual route. 

With relation to language complete word-blindness is shown by in- 
ability to read or write. The patient cannot read because he cannot 
recognize the characters before him. He cannot write because he cannot 
recall the shapes of the necessary letters. If the defect be only partial, 
he can write at dictation or copy, although not understanding what is 
written. 

Complete word-blindness indicates a cortical lesion in the region 
of the inferior parietal convolutions and angular gyrus. A partial 
word-blindness is produced by a sub-cortical lesion involving the fibers 
of association. 

3. Intercortical Sensory Aphasia. — The fibers of association be- 
tween the auditory and visual word centers may be interrupted, pro- 
ducing a condition in which an object seen cannot be named, or if named 
cannot be recalled to mind, although recognized in both instances. This 
condition is produced by lesions of the association fibers connecting the 
temporal and occipital lobes. 

2. i\IoTOR Aphasia. — 1. Aphemia, or what is commonly called sim- 
ply aphasia, a condition in which although words or things are recog- 
nized by eye and ear, the patient cannot name them or speak because 
of inability to recall the muscular movement necessary. This happens, 
■of course, independent of paralysis of the muscles of speech. 2. 
Agraphia, the condition in which one can name objects and speak as 
usual, but cannot write, because the memory of the movements neces- 
sary is lost. 3. Iidercortical motor apliasia or paraphasia. In this 
condition an interruption or interference with the association fibers 
connecting the motor and other word-memory centers results in a dis- 
turbance characterized by the use of the wrong Avord in speech or 
writing. The patient speaks or writes jargon. Paraphasia is particu- 
larly associated with lesions of the island of Reil. 



PLATE VII. 




The Fundus in Amaurotic Family Idiocy. 



AMAUROTIC FAMILY IDIOCY 



549 



AMAUROTIC FAMILY IDIOCY 

Definition. — A rare affection of Hebrew children, characterized by 
mental impairment during the period of infancy, blindness and loss of 
power over much of the body. 

Etiology. — The causation is unknown. The disease occurs only 
among the Hebrews, and often affects more than one child in a family. 
It is not syphilitic. 

Morbid Anatomy. — A degenerative process is found affecting all 
the nerve-cells of the brain and cord. The degeneration affects particu- 
larly the body of the cell and the dendrites, not the axis cylinder. The 
changes in the cell may be slight or so complete that the cell is disin- 
tegrated. Sachs thinks the disease due to congenital deficiency of the 
nervous system, such that after three or four months of normal life, 
the cells yield to the ordinary demands of life and disintegrate. 

Symptoms. — These are briefly summed up by Sachs as: (1) Mental 
impairment during the first few months of life leading .to complete 
idiocy. (2) Paresis or paralysis, either flaccid or spastic, of the greater 
part of the body. (3) The reflexes may be deficient, normal or in- 
creased. (4) A diminution of vision terminating in absolute blind- 
ness. (5) Marasmus and death before the age of two years. 

Various other symptoms, such as increased sensibility to touch or 
sound, nystagmus, strabismus, or convulsions, have been noted in some 
eases. 

Diagnosis. — This rests upon the mental impairment, the blindness 
and the ophthalmoscopic examination, which shows, in the region of the 
macula lutea, a bright cherry-red spot, an absolutely pathognomonic 
sign. (See Plate VII.) Treatment is of no avail. 

FUNCTIONAL NERVOUS DISEASES 

ACUTE DELIRIUM 
(Typhomania. Brain Fever. Bell's Mania) 

Definition. — An acute delirium or mania accompanied by fever, 
regularly fatal, without adequate organic lesions. 

Etiology. — Emotional excitement, injury, toxemia and infection are 
given as causes. In most instances no satisfactory explanation is to 
be had. 

Morbid Anatomy. — The meninges are congested, but the brain 
appears normal. Microscopically Osier found some exudation of leu- 
kocytes about the vessels and in the lymph-spaces. 

Symptoms. — The onset may be preceded by several days of restless- 
ness, irritability and insomnia. The onset is usually marked by fever, 
102° to 104° F., with some increase in the pulse and prostration. Wild 
delirium or an active mania develops easily. Hallucinations are vivid, 
the patient talks or sings incessantly, and keeps in constant motion. 



550 



FUNCTIONAL NERVOUS DISEASES 



Such acts as salaaming may be repeated endlessly. The patient may 
struggle with his attendants, but rarely injures anyone but himself. 

A typhoid-like condition is developed with fever, a dry-brown 
tongue, rapid pulse, marked prostration, and rapid emaciation. At the 
end of a week or ten days the patient dies in collapse. 

Diagnosis. — Typhoid fever must be excluded by absence of the 
characteristic roseola and the enlargement of the spleen, and by the study 
of the leukocyte count, the V^^idal reaction, and blood cultures. Pneu- 
monia can be excluded only by the absence of the usual symptoms and 
repeated careful physical examinations. Delirium tremens presents a 
distinct etiology, characteristic hallucinations, and the active tremor of 
tongue and hands. 

Acute meningitis may be excluded by the absence of rigidity of the 
neck and Kernig's sign, and by the results of lumbar puncture. It is 
evident that, the diagnosis of acute delirium can hardly be safely ven- 
tured before the autopsy reveals the absence of lesions sufficient to 
account for the disease. 

Treatment. — Blood-letting has been recommended in the early 
stages. The general treatment must be that of typhoid fever. The 
bromides gr. xxx t. i. d. may be given for excitement or hyosein in doses 
of 1/100 gr. Dram doses of the fluid extract of ergot every two hours 
are recommended. 

PARALYSIS AGITANS 

Definition. — A chronic nervous affection marked by muscular weak- 
ness, tremors and rigidity. 

Etiology. — Two-thirds of the patients are men. The disease rarely 
begins before forty. Exposure, privation and nervous strain appear 
to favor its development. Numbers of cases were observed during the 
siege of Paris and the war of the rebellion. 

Morbid Anatomy. — No distinctive lesions have been found. Brawny 
patches in the skin have suggested myxedema, and the theory that 
lesions of the parathyroids were related to the disease has been ad- 
vanced. 

Symptoms. — The onset is either sudden or gradual. Usually the 
weakness, stiffness and tremor appear in one hand or arm, then the 
other. All four extremities and even the head may be affected. When 
fully developed the clinical picture includes: 

1. The tremor, the most striking symptom. It is a rapid tremor, 
four to eight oscillations per second, usually most marked in the hand. 
The movement of the fingers suggests pill-rolling. Flexion and exten- 
sion of the wrist or slight rotation may be combined with the finger 
movements. It may show clearly in the hand-writing. It usually is 
present at rest, and disappears on effort, but in some cases accom- 
panies voluntary action — i.e., is intentional. In the foot the tremor 
causes rapid flexion and extension at the ankle, and the toe taps the 
floor as in clonus. 



ACUTE CHOREA 



551 



2. Rigidity of the muscles is the most pronounced feature of the 
disease. Rigidity precedes or accompanies the tremor. Passive motion 
may be impeded, but the reflexes are not increased and ankle clonus 
is not found. The facies becomes mask-like. The eyes are held 
open and fixed in one position, the whole head being revolved in- 
stead of moving the eyes from side to side. The patient rarely 
winks. The neck muscles are rigid as in torticollis, but both sides 
are involved, and the face is not turned to either side. The body 
is bent forward at the hips and the spine is bowed forward. In 
the hands similarly the fingers and wrists are usually flexed. Speech 
and gait are often characteristic. In speaking the patient hesi- 
tates a moment, then hurries the words out and stops abruptly. In 
like manner the patient, rising from a chair, halts a moment, then with 
the body bent forward advances with short, hurried steps, as though 
the feet were trying to overtake the body. In rare cases the patient 
actually falls forward. 

3. The mental state is marked by inertia. The patients are dull, 
sluggish, talk little and are indifl^erent. Dementia is often sug- 
gested, but when roused the patients show complete possession of their 
faculties. 

4. Sensory disturbances. The patients complain of sensations of 
heat or cold, but respond normally to tests. Vasomotor changes may 
be indicated by flushing of the skin, increased sweating or salivation. 

5. Muscular atrophy is not marked and no electrical changes are 
present. 

Course. — The disease is chronic and incurable, lasting many years. 
Periods of improvement may occur. 

Diagnosis. — In a typical case the diagnosis can be made on sight. 
The attitude of the body, the gait, the mask-like face, and muscular 
rigidity as well as the tremor are characteristic. Disseminated sclerosis 
is marked by earlier onset, scanning speech, and nystagmus. The 
tremor is regularly intentional. Post-hemiplegic tremor can be ex- 
cluded by the history of preceding paralysis and the increased reflexes. 
Hysteria must be considered. 

Treatment. — Medication appears to be of no avail. Massage, elec- 
tricity and vibration have been of service. The administration of ex- 
tracts of the parathyroid glands has been advised. 

ACUTE CHOREA 
(Chorea Minor. Sydenham's Chorea. St. Vitus' Dance) 

Definition. — A nervous affection, common in children, characterized 
by irregular involuntary muscular contractions, resulting in purpose- 
less movements, and often accompanied by psychic disturbances. 

Etiology. — The disease is common between the ages of five and fif- 
teen, especially in girls. A neurotic heredity can often be traced. The 
strain of school-life is usually the chief factor. Sudden fright or ex- 



552 



FUNCTIONAL NERVOUS DISEASES 



citement often precedes the appearance of symptoms. About 25% of 
the patients give a history of antecedent rheumatism. Any acute in- 
fectious disease or other condition lowering the vitality of a child may 
be an accessory cause of chorea. 

Morbid Anatomy. — Death from chorea is rare and pathological 
studies relatively few. Minute emboli in the cerebral vessels have been 
found in some cases, and have led to the theory that chorea is caused 
by numbers of such emboli taking their origin from a rheumatic endo- 
carditis. This theory covers but a part of the cases. 

Perivascular hemorrhages and areas of infiltration in the brain have 
also been observed. The pathology is by no means established. 

Bacteria. — Many investigators have found bacteria in the brain, 
but the organisms have been of wide variety, usually streptococci. 
Poynton and Paine found their streptococcus rheumaticus in the cere- 
bral embolisms. The dependence of the disease upon bacterial infec- 
tion is not established, but the theory that it is due to the action of 
toxins, probably bacterial, upon a sensitive nervous system receives much 
support. 

Symptoms. — Motor. — Irregular, jerky, purposeless movements of 
one or both upper extremities are first noted. The movements may be 
confined to one extremity or extend to all. The face may be affected. 
With these movements awkwardness and weakness in the use of the 
hands or other parts develop. The patient drops things because of the 
chorea and is often rebuked or punished for carelessness. Speech may 
become hesitating, jerky and imperfect. The movements may be very 
slight, occurring at rare intervals and for some time scarcely attract- 
ing attention. In the mild form they cease during sleep. They are 
regularly increased by excitement or embarrassment, and are there- 
fore often most noticeable during examination. In severe cases the 
jerky movements affect all parts of the body, are almost constant, more 
violent, and may persist during sleep. The weakness may develop into 
paralysis. 

Psychic. — Irritability, peevishness and inability to concentrate the 
attention attend the milder cases. In severer forms the mental dis- 
turbance becomes more marked. Delirium with varied hallucinations 
may develop. Stupor and dementia have been observed in fatal cases. 
Constitutional anemia, malnutrition and loss of appetite are regularly 
present. The pulse is rapid and the patients feeble. Fever appears 
only in the severer cases. 

Complications. — Heart murmurs are common. They may be 
hemic or due to definite endocarditis. The location of the apex impulse, 
the size of the heart, the character of its action, and the circulatory 
conditions must all be considered in attempting to decide this question. 
Acute pericarditis occasionally develops. Other rheumatic complica- 
tions, such as erythema nodosum, purpura and subcutaneous nodules, 
may be seen. 

Course. — The disease runs its course in two or three weeks or 



CONVULSIONS OF CHILDREN 



553 



months. It regularly ends in recovery. Occasional choreic movements 
may be seen for months afterward. Death is possible in the severe 
forms. 

Treatment. — Freedom from disturbing influences of any kind, fresh 
air and good food are the prime requirements. The home conditions 
must be made favorable or the child removed from them. Relief from 
school duties, an out-door life, and nutritious food will promptly re- 
lieve mild cases. In pronounced cases rest in bed is necessary. 

Arsenic is regularly administered. Fowler's solution in doses of 
2 to 5 minims, thrice daily, is commonly given. Some increase the dose 
to the limit of intolerance, but this seems undesirable. 

Chloral and the bromides are often given for sedative effect. Massage 
8.nd passive movements may be employed. In chronic cases suggestion 
and educative exercises are of value. 

CONVULSIONS OF CHILDREN 
(Infantile Convulsions) 

Definition. — General tonic and clonic convulsions occurring in child- 
hood from various causes, not including epilepsy. 

Etiology. — A family tendency to nervous disturbance is notable in 
some cases ; in others the individual seems to have an abnormally sensi- 
tive nervous system. The origin of this weakness can often not be 
made out. In children of such hereditary or acquired nervous suscep- 
tibility any form of trauma, toxemia or infection may be the cause of 
a general convulsion. The possible causes of convulsions in childhood, 
therefore, include practically all the varied forms of disease or injury 
to which they are subject. Certain influences are so important as to be 
specially enumerated. 1. Gastro-intestinal disorders of any kind, espe- 
cially overloading the stomach with indigestible food, and constipation, 
are the commonest causes of convulsions in childhood. Intestinal para- 
sites and inflammations of any kind are important factors. 

Dentition is commonly regarded as the most frequent cause of in- 
fantile convulsions. In most instances it is some associated alimentary 
disorder and not the "cutting of the teeth" that causes the disturb- 
ance, yet in very sensitive children "teething" alone may cause con- 
vulsions. 

2. In childhood the invasion of an acute infectious disease, espe- 
cially pneumonia, scarlet fever, whooping-cough or small-pox, is fre- 
quently marked by a convulsion. The initial chill commonly seen in 
adults at the onset of such acute infections seems to be replaced in 
childhood by a convulsion. 

3. Rachitis predisposes children to convulsive seizures. 

4. Any illness or indisposition lowering the vitality of a child favors 
these convulsive seizures. 

5. Fright or excitement may precipitate a convulsion in a suscepti- 
ble child. 



554 



FUNCTIONAL NERVOUS DISEASES 



Symptoms. — The convulsions may occur in a child apparently in 
perfect health or they may be preceded by irritability and restlessness 
with evidences of digestive disturbance. 

The seizures vary from attacks of brief unconsciousness with little 
or no spasm to general tonic and clonic convulsions not to be distin- 
guished from the characteristic fits of epilepsy. 

In the milder attacks, the so-called "inward spasm," the child be- 
comes silent, rigid, stares or rolls the eyes upward, the face or one hand 
twitches for a moment and the paroxysm is over. 

The severer paroxysms begin in like manner, but the whole body 
becomes rigid, the hands clinched, the elbows flexed, the head retracted, 
and quick spasmodic jerkings of the face and extremities follow. The 
respiration is embarrassed, the pulse becomes rapid, feeble, and possibly 
imperceptible. The face and lips become deeply cj^anosed and death 
appears imminent. There may be frothing at the mouth and rattling 
of mucus in the throat. After lasting a few seconds or several minutes 
the convulsion gradually ceases, the muscles relax, and the child passes 
into a stupor from which it rouses slowly, perhaps hours afterward. 
The attacks may be repeated at any time ; frequently several follow one 
another at short intervals, and many may occur in a day. Death rarely 
follows a single convulsion, but may result if the convulsions are fre- 
quently repeated. 

The convulsions are likely to recur, but may not. In most cases they 
cease entirely as the child grows older. Persistence of the convulsions 
usually means epilepsy. 

Diagnosis. — The convulsion can be recognized on sight or history. 
The cause is the important question and must be sought with care. A 
thorough physical examination and a study of the diet and life of the 
child should be made to determine the conditions which have caused 
the convulsions. Epilepsy can be excluded only after prolonged ob- 
servations, but it is to be remembered that convulsions are common, 
epilepsy in infancy relatively rare. 

Treatment. — During the convulsion chloroform should be given by 
inhalation. If the tongue is protruded or caught between the teeth a 
bit of wood or rubber should be used as a gag to prevent injury to it. 
A hot bath or hot pack, with mustard added to the water in the propor- 
tion of a tablespoonful to the gallon, should be given at once with the 
object of reducing internal congestion by bringing the blood to the 
surface. The bowel should be emptied by an enema, and castor oil given 
by mouth. Chloral and the bromide of soda may then be given by 
rectum, 5 grains of chloral and 10 of the bromide to a child of a year 
or more. If the danger of recurrence seems great, morphine sulphate, 
gr. 1/50 for a child of one year, may be given hypodermatically. 

Quiet and a restricted diet should be required for several days be- 
fore allowing return to the ordinary mode of life. Careful examina- 
tion should then be made for any possible cause of convulsions. The 
diet and regulation of the life are of prime importance. Rachitis if 



EPILEPSY 



555 



present must be treated. Adenoids may require removal. Anemia 
should be treated, and in every way the general health of the child 
maintained at the highest point. Excitement or excess of any kind 
must be avoided. If under such care convulsions are repeated the prob- 
ability of epilepsy is increased. 

EPILEPSY 

Definition. — A nervous affection characterized by periodic attacks 
of unconsciousness commonly associated with general convulsions and 
frequently preceded by an aura. 

Etiology. — Epilepsy regularly develops in childhood in either sex, 
and rarely begins after the age of thirty. Heredity plays an important 
part. If epilepsy itself is not present in the family, neuroses of some 
kind are often found. 

Syphilis, tuberculosis or alcoholism in the parents predisposes to 
epilepsy. Every influence which lowers the nervous vigor of a family 
favors the development of epilepsy. Similarly any influence which 
lowers the nervous vigor of the individual may in a susceptible person 
precipitate the first attack or cause the repetition of the convulsions, 
(a) Toxic influences, such as alcohol, tobacco, or the toxemia resulting 
from overburdening the alimentary tract and constipation, are of first 
importance, (b) Acute disease of any kind, especially the acute in- 
fectious diseases, may precede the onset, (c) Reflex irritations from 
eye-strain, adenoids, intestinal parasites, uterine or ovarian disease, 
phimosis and the like, (d) Mental shock or excitement are important 
agencies, (e) In females the attacks are likely to occur at the time of 
menstruation. 

The cerebral hemorrhages of birth, injuries to the skull at that time 
or later, defective cerebral development from any cause, all favor 
epilepsy. Idiocy or imbecility and epilepsy are frequently associated. 

Morbid Anatomy. — Many brain lesions have been found in patients 
suffering from epilepsy, especially defects of development, poren- 
cephalus, hemorrhage, cysts, tumors, meningitis and the like. These 
lesions are not essential, however, but may be regarded as sources of 
irritation which favor the development of convulsions. Recently care- 
ful studies have shown that in those dying of epilepsy degenerations in 
the cerebral nerve-cells, especially those of the second cortical layer, 
can be demonstrated. These degenerations involve especially the nuc- 
leus and nucleolus. 

Epilepsy is still, however, regarded as a functional disease— 
without definite anatomical basis. 

Symptoms. — 1. Grand Mal. — The seizures of general convulsions 
are the typical form of the malady. These include a tonic stage, a clonic 
stage, and a period of stupor or coma, and in many cases are preceded 
by an aura. 

The Aura. — A warning of some kind occurs in many cases ; it may be 
motor, sensory or psychic. Motor. A tremor, a jerk or movement of 



556 



FUNCTIONAL NERVOUS DISEASES 



some part or parts of the body, rapid revolution, or running forward 
a few steps are sometimes seen. Sensory aurie are more common. 
Tingling, burning, numbness, a certain sound, a flash of light and various 
other unusual sensations are recorded. Psychic aurge present them- 
selves as a certain mental depression or exaltation, certain emotions, 
or recollections. Whatever the aura it is repeated, as a rule, before 
each fit. The aura may just precede the paroxysm, but sometimes an 
interval of some minutes elapses before the onset. Aurse are present in 
a majority of patients but not in all. 

Tonic Stage. — The patient suddenly becomes unconscious and falls, 
often injuring himself about the head and face in falling. The whole 
body becomes rigid. The head is drawn back or to one side, the eyes 
are turned upward and to one side, the face is pale, the thorax immov- 
able (apnea), the limbs flexed. Often the sudden contraction of the 
respiratory muscles causes an inarticulate cry. The tonic stage lasts 
but a minute or two. 

Clonic Stage. — The convulsive movements begin in the face or an 
extremity, but quickly become general. The eyes, face, limbs and whole 
body are thrown into violent jerky contractions, the teeth are ground 
together, the tongue is protruded and often bitten, the saliva is churned 
into froth and pours from the mouth, the respiration is jerky and im- 
perfect, the face becomes cyanotic, the pulse rapid and weak. The 
contractions last from one to five minutes, and then gradually die out. 
Both bladder and rectum are commonly evacuated during the paroxysm. 
Stupor or complete coma follows, lasting a half hour or more. The 
patient then awakes, possibly unconscious that he has had a convulsion, 
but usually weak, depressed and mentally confused. 

Recurrence. — Epileptic fits recur after varying intervals, hours, days, 
months or years. The fits often occur in groups. Fright, fatigue, ex- 
citement and the like may precipitate an attack, but usually they recur 
without apparent cause. In most cases the attacks slowly increase in 
frequency. 

Nocturnal epilepsy is common, the fits coming on at any time dur- 
ing the night, even in sleep. Under these circumstances the patient may 
not know what has happened or may be aware from the muscular sore- 
ness, exhaustion or the bitten tongue that he has had a fit. 

Status Epilepticus. — In some instances, especially late in the dis- 
ease, the fits are repeated in a long series, are accompanied by fever, 
even 104° to 105° F., and followed by collapse. Such crises end favor- 
ably, as a rule, but death may occur. 

Postepileptic State. — Usually the mind quickly clears, but it may re- 
main clouded. A trance-like condition may supervene, and mania with 
homicidal tendencies is well known to follow in some cases. 

2. Petit Mal. — Temporary unconsciousness with few or no convul- 
sive signs marks this condition. The manifestations are varied. In some 
a sudden pallor, a fixed stare, a momentary obliviousness, are all that 
are seen. Slight tremor of the eyes, face or an extremity may be seen. 



EPILEPSY 



557 



The patient may fall or may drop what he is holding. The urine may 
be passed involuntarily. 

In other cases the patient turns rapidly about, or runs a few steps 
in an automatic manner, and then returns to his usual condition. 

Psychic Equivalents. — In rare cases the epileptic seizure is replaced 
by some unconscious and automatic act. Murder has been done, and 
tires set by the irresponsible victims of such seizures. In other cases 
long journeys have been taken or various complicated acts performed. 
Ordinary convulsions occurring before or after such paroxysms reveal 
their nature. 

Course. — The disease tends to grow worse with steady increase in 
frequency of the convulsions and Increasing mental dulness in the in- 
tervals. The patients may die from their falls or injuries received 
while unconscious (drowning) or from the convulsions, or in a condi- 
tion of dementia. 

Diagnosis. — The typical fit can hardly be mistaken. The aura, tonic 
and clonic spasm and subsequent stupor are very characteristic. Repe- 
tition of the convulsions is highly suggestive. The presence of scars 
or bruises on the scalp or the tongue is helpful. Nocturnal fits are regu- 
larly epileptic. In children under two years convulsions are often re- 
peated a number of times and then cease, without subsequent epilepsy. 
The family history is important, but time is required to settle the ques- 
tion. In adults the convulsions of uremia are sometimes mistaken for 
epilepsy. The anemia, cardiac changes, arteriosclerosis and urinary 
findings should differentiate the condition. 

Hysteria is easily recognized. The fit is overdone. The patient is 
noisy, never injures himself or herself, but may strike others ; the con- 
vulsion is exaggerated, unconsciousness is feigned, but there is no 
relaxation of the sphincters and no coma. 

3. Jacksonian Epilepsy. — (Cortical, symptomatic or partial epi- 
lepsy.) In this condition the seizures are limited to one extremity or 
to one side of the face. The convulsion may extend from one part to 
another, as from the arm to the leg or vice versa. The localized form 
may at any time give place to a general convulsion. Jacksonian epi- 
lepsy usually arises from focal irritation of the brain, such as a de- 
pressed fracture, a localized meningitis, a tumor or abscess. Similar 
attacks may occur in uremia. The location of the focal lesion is usually 
indicated by the part in which the convulsion begins. 

Prognosis. — Some few patients recover, but the disease is generally 
incurable and tends to be progressive. 

Treatment. — General. — The patient must be examined thoroughly 
for any defect which may be a source of irritation. Eye-strain, aden- 
oids, uterine displacement, any possible source of local irritation should 
be relieved. The digestion should be studied, an easily digestible diet 
prescribed, and constipati(m avoided. An out-door life with freedom 
from annoyance or care is helpful. Moderate exercise is desirable. 
Excess of any kind must be forbidden. 



558 



FUNCTIONAL NERVOUS DISEASES 



Medicinal. — Bromide of potassium or sodium is effective in reduc- 
ing the frequency of the paroxysms. Small doses, 5 grains, are given, 
and the dose later increased. If acne appears, the medicine must be 
reduced or stopped. It may be continued indefinitely. ]\Iany other 
nerve sedatives, chloral, cannabis indica, zinc, etc., are employed. 

Institutional. — Control of the mode of life of the epileptic patient 
is essential. If this cannot be secured at home, removal to a sanatorium 
should be urged. Great numbers of epileptic patients are now treated 
advantageously in farm-colonies, such as the Craig Colony. Sonyea, 
N. Y. Jacksonian epilepsy may be relieved by trephining and appro- 
priate treatment of the focal lesion. 

MIGRAINE 
(Megrim. Sick Headache) 

Definition. — An affection characterized by attacks of severe head- 
ache, often attended by disturbances of vision and digestion. Migraine 
presents a close analogy to an epilepsy in which the motor discharges 
are replaced in large part by sensory phenomena. 

Etiology. — The explanation of migraine is regularly based on two 
factors, a constitutional nervous defect or weakness, and some local dis- 
turbance or weakness, (a) Constitutional. Heredity is regarded as 
important. Some neuropathic taint (headaches, epilepsy, neurasthenia 
and the like) can usually be found in the family. A gouty tendency is 
sometimes present and excess of uric acid in the blood or deficiency of 
it in the secretions is commonly invoked as explaining the attacks of 
megrim. Exact proof of the relation of either of these conditions to 
megrim is, however, lacking, and the common accusation of uric acid 
in this regard is without adequate foundation. 

(b) Local conditions. These comprise most functional and organic 
defects, such as simple constipation, eye-strain, adenoids, nasal spurs 
and polypi, uterine or ovarian disease and the like. In general any 
influence which lowers the health of the patient or acts as a source of 
local irritation may have relation to attacks of migraine. In many cases 
it is quite impossible to determine the etiology. The affection appears 
in families without neuropathic taint and in healthy individuals. The 
attacks begin in childhood or early adult life, more often in females. 

Symptoms. — Prodromal disturbances announce to some the ap- 
proaching attack. The prodromata are varied, languor, drowsiness, 
flashes ot light, spasm of ocular muscles, dilatation of the pupil and the 
like. The headache itself usually begins in the morning. The pain is 
referred to any part of the head, usually unilateral, sometimes sharply 
localized. Visual disturbances commonly accompany the pain. The 
sight is blurred, or there may be definite hemianopsia. 

In some eases varied figures with flashing colore play before the 
eyes. Nausea and vomiting are common : the vomitus is yellow from 
the presence of bile. Vomiting is severe in some persons and may give 
relief. 



NEURALGIA 



559 



Tingling and numbness may be felt in the face or arm, and may 
be accompanied by wealmess or actual loss of power. Speech may be 
slow and stumbling and temporary aphasia may develop. The face is 
usually pale from vasomotor constriction, and later the face and ear 
on the affected side may flush. The patient is greatly prostrated and 
hypersensitive to noise or disturbance of any kind. The attack usually 
lasts throughout the day or several days. The patient is prostrated for 
some time afterward. 

Course. — The attacks occur at intervals of days or weeks, sometimes 
from definite indiscretions in diet or life, but often without apparent 
reason and despite the best of treatment. They tend to become less fre- 
quent and less severe in later life. The menopause seems to bring relief 
to women. Many patients having sought relief in vain finally resign 
themselves to their suffering, and yet are able to live lives of activity 
and usefulness. 

Treatment. — The Attack. — A brisk saline cathartic taken at the 
first signal of the attack is advisable. Washing out the stomach with 
hot water is recommended in those cases where vomiting is severe. 
Black coffee given at the onset is sometimes helpful. During the attack 
the patient must be kept in bed and heat applied to the feet. Acetanilid, 
phenacetin and caffeine are given for relief of the pain, and are some- 
times helpful, if they can be retained. Morphine may be required for 
the very severe attacks, but should be withheld, if possible. Often the 
after-effects of morphine are so disagreeable to these patients that its re- 
lief is declined. Hot or cold applications, as preferred, may be made to 
the head. 

General. — In the intervals the life of the patient should be carefully 
planned. A vegetarian diet helps some, but dietary restrictions are 
usually valueless. Avoidance of such articles of food as cause gastric 
disturbance usually commends itself to the patient. Excesses of any 
kind should be avoided. Abundance of sleep and rest is advisable. An 
out-door life and moderate exercise are recommended. 

Local. — Every defect should, if possible, be corrected. Thus errors 
of refraction, adenoids, bad teeth, digestive disturbances, especially con- 
stipation, uterine or ovarian disease and the like must be appropriately 
treated. 

NEURALGIA 

Definition. — A painful affection of a nerve or nerves without dis- 
coverable lesions either in the nerve itself or adjacent tissues to ex- 
plain it. 

The term is a broad one which commonly is loosely used to cover all 
types of pain. Every effort should be made to distinguish neuralgia, on 
the one hand, from pain excited by definite nerve changes such as occur 
in neuritis, and on the other from pain due to definite local lesions, such 
as abscesses, new growths and the like. Even with the most careful 
study, however, we may be unable in some cases to distinguish neuralgia 
from neuritis. 



560 



FUNCTIONAL NERVOUS DISEASES 



Etiology. — The affection is rarely met with in childhood, but is com- 
mon among adults, especially women. A neurotic tendency or heredity 
underlies many cases. The weak and anemic are most subject to it. 
Constitutional conditions producing weakness and anemia may precede 
it, especially infectious diseases, such as influenza and malaria, or the 
systemic poisons of rheumatism, gout, diabetes or chronic nephritis, or 
alcohol, lead or arsenic. In those liable to the affection, exposure to 
cold and wet, or any condition producing nervous exhaustion or debility 
may precipitate an attack. In not a few cases no cause can be found 
and we must be satisfied to call them idiopathic. The term ought not 
to be applied to pains which can be explained by definite pathological 
lesions, such as caries of the teeth, suppuration in the antrum of High- 
more, pressure of tumors and the like. The more carefully patients are 
studied the less use we shall have for this designation. 

Symptoms. — Neuralgia presents itself in the form of paroxysms of 
pain, usually described as sharp, burning or stabbing, in the territory 
of a certain nerve or nerves of one side of the head or body. The 
paroxysms last for a brief time or may be protracted. In the intervals 
there is usually no discomfort. The pain is usually severe, and may be 
agonizing. Regularly there are no changes seen in the affected area. 
There may, however, be vasomotor or finally trophic changes in per- 
sistent cases. Thus the skin may be hot and red, or cold and pale. 
Edema, atrophy or induration of the skin, or whitening of the hair in 
chronic cases may be seen. "Where herpes or such changes as these are 
met with we are probably dealing with manifestations of definite lesions 
of the nervous system. (See Herpes Zoster.) 

The attacks of pain are likely to recur at regular intervals of a day 
or days, without relation to malaria. The pain often shifts from one 
nerve to another. Along the course of the affected nerve there may be 
tender points, especially where it emerges from a canal or becomes more 
superficial. The affection lasts for varying periods, weeks or months, 
or in some cases persists for life. Any nerve in the body may be affected. 
The more important varieties follow: 

(1) Trigeminal Neuralgia. Tic Douloureux. Any of the branches 
of the fifth nerve may be involved. The attacks of pain are character- 
istic. The affection is often severe and protracted, and may require 
heroic measures for relief. Before accepting the diagnosis of neuralgia 
we must carefully exclude organic lesions, such as the pressure of tumors, 
cerebral or in the course of the nerve, disease of bone causing pressure 
in the course of the nerve, or any cause of peripheral irritation, such as 
caries of the teeth, suppuration of the antrum or the frontal or ethmoidal 
sinuses, or the growth of tumors within the orbit, nose or mouth. In 
neuralgias of the ophthalmic division the possibility of glaucoma, or 
errors of refraction or muscular defects of the eyes must be considered. 

(2) Intercostal Neuralgia. — This is frequently a severe type of 
the affection. Care must be taken to exclude pressure on the nerve by 
diseased vertebrie (Pott's disease) or aneurisms or other tumors. Pleurisy 



NEURALGIA 



561 



or other inflammatory lesions must be ruled out. The association with 
herpes zoster is frequently seen in this form of the disease. 

(3) Lumbar Neuralgia. — Lesions of the spine, of the kidney or 
other abdominal viscera must be sought for, stone in the kidney espe- 
cially. Herpes zoster is frequent in this type also. 

(4) Neuralgia of the Upper Extremity. — Here we must look par- 
ticularly for causes of pressure upon the brachial plexus or the nerves 
of the arm, involvement of the shoulder- joint or adjacent bursa, and 
remember that neuritis is much more common than neuralgia. 

(5) Neuralgia of the Lov^er Extremity. — Sciatica is considered 
separately. For neuralgic pains in the feet we most often find explana- 
tion in the presence of affections of the arch (flat-foot) or disease of 
the bones (especially tuberculosis). The metatarsalgia of Morton is a 




FiG. 109. — Herpes zoater, lesion of lower lumbar nerves. A, fresh lesions; B, older, drying lesions 

and pigmentation. 



neuralgic affection usually due to pressure upon one or more of 
the nerves of the foot. The possibility of locomotor ataxia is to be 
remembered. The condition of the veins and arteries must be con- 
sidered. 

(6) Herpes zoster is a neuralgic affection of the intercostal nerves 
dependent upon an acute interstitial inflammation of the dorsal root 
ganglia and therefore not properly included among functional affec- 
tions. Clinically it is, however, best considered in this relation. The 
affection is characterized by an attack of pain referred to the territory 
of one or two intercostal or lumbar nerves on one side of the body, asso- 
ciated possibly with slight fever and constitutional disturbance. The 
skin of the affected area is hyperalgesic. After three or four days an 
eruption of many fine vesicles appears along the course of the nerve, 
usually in several scattered groups, sometimes extensive (see Fig. 106). 
36 



562 



FUNCTIONAL NERVOUS DISEASES 



In the course of a week or ten days the vesicles diy up and disappear, 
leaving brownish pigmentation and in some instances minute scars. As 
a rule the pain lessens with the development of the eruption and ceases 
with its disappearance ; in rare instances it persists indefinitely. 

Diagnosis. — The common organic causes for pains often called neu- 
ralgia have been suggested. Neuralgia must also be distinguished from 
neuritis. The latter affection can usually be recognized by more general 
tenderness along the course of the nerves, the presence of marked trophic 
or vasomotor changes, loss of sensation or paralysis in the affected part 
or the electrical reactions of degeneration. 

Prognosis. — Usually the affection is readily amenable to treatment. 
It may, however, prove protracted, and in the severer types, suicide is 
not unknown. The affection is never fatal in itself. 

Treatment. — (1) Constitutional. — The adequate treatment of de- 
bility and anemia is essential. Rest, fresh air, good food and tonics, such 
as iron, str^^chnine, quinine, cod liver oil, the hypophosphites, or glycero- 
phosphates may be employed. In the poorly-nourished forced feeding 
is advantageous. In severe cases a favorable climate and agreeable 
surroundings are helpful. The withdrawal of the use of alcohol or 
any other poison, such as lead or arsenic, is indicated. Influenza, 
malaria, rheumatism, gout or diabetes, if present, must be properly 
treated. 

(2) Symptomatic. — The relief of the attacks of pain, (a) The 
common analgesics, aspirin, phenacetin, antipyrin or antifebrin may be 
given in appropriate doses. The possibility of harm from their use, 
especially if continued for any length of time, must be borne in mind. 
Their effects on the heart and circulation should be carefully watched. 
Strychnine given in full doses hypodermatically is sometimes valuable. 
Aconitia, in doses of 1/200 to 1/150 grain may be tried, and is a success- 
ful but also a dangerous remedy. JMorphine should be used only when 
everything else has failed. The danger of a"^ habit is great, (b) Local 
treatment. Applications of heat or cold (the hot-water bottle or ice- 
cap) may be of help. Various anodyne liniments are employed, such 
as chloroform, belladonna, chloral and camphor, menthol. The actual 
cautery is valuable, where it can be used, as on the trunk or extremities. 
The galvanic current may be*of service. 

Surgery is the last resort. Division of the affected ner^^e, or resec- 
tion, or finally the excision of the ganglia, in the case of the fifth nerve, 
the Gasserian, may be required. 

TETANY 
(Tetanilla) 

Definition. — A rare affection characterized by intennittent tonic 
cramps of the extremities, often painful, and usually without constitu- 
tional or cerebral disturbance. The condition is a symptom-complex 
(rather than an independent disease), associated with a great variety 



TETANY 



563 



of conditions varying from parathyroidectomy to intestinal infections. 

Etiology. — This condition has recently been demonstrated to be dne 
to a poverty of the blood and tissnes in calcium salts caused by loss of 
function on the part of the parathyroid glands. The peculiar localiza- 
tion of the spasms is a^ yet unexplained. 

Tetany is met with at all ages, but especially in children. It has 
been observed in many different conditions, but is most often seen in 
(a) gastro-intestinal disease in children, especially the rachitic, (b) 
dilatation of the stomach in adults, (c) in pregnancy, and (cl) follow- 
ing thyroidectomy, the parathyroids being unwittingly removed with the 
larger gland. 

The parathyroids in man vary from two to four in number, and are 
minute glandular bodies lying in close relation to the posterior border 
of the thyroid, and therefore easily removed with it. 

Symptoms. — The cramps first appear in the hands, later in the feet. 
Escherich insists that in children the larynx is frec|uently involved, and 
instances of involvement of the face and thoracic muscles are known, 
but the manifestations are commonly limited to the hands and feet. The 
cramps are bilateral and symmetrical. In the upper extremity the 
wrists are flexed, the thumb is drawn into the palm, the fingers flexed 
at the metacarpo-phalangeal joints but otherwise straight, giving the ap- 
pearance known as the accoucheur's hand. In the lower extremity the 
foot is partly extended, unusually arched, the toes turned inward and 
closely adcluctecl. Various modifications of the attitude of the hand 
may be observed, especially that in which the thumb is drawn strongly 
into the palm and the fingers flexed upon it. The spasm is tonic, inter- 
mittent, and can be excited by various forms of irritation, mechanical 
or electrical. The spasm is increased by pressure upon the nerves or 
arteries of the affected limb (Trousseau's sign), indeed by pressure 
anywhere upon the limb, or even the opposite member. The electrical 
excitability of the muscles is increased (Erb's sign). Tapping over 
a nerve or upon a muscle excites spasm in the affected muscles (Chvos- 
tek's sign). Chvostek's sign is best brought out by tapping the facial 
nerve in front of the ear. Much has been made of these special signs, 
but they are not constant and are not always easily elicited. Trous- 
seau's sign is most reliable. The sensory nerves have also been sho\\Ti 
to be easily excited. 

The spasms in the extremities come and go, enduring for a varying 
length of time, lessening as the primary condition improves in cases of 
gastro-enteritis, or persisting till death in fatal cases. The condition 
when seen in adults with gastrectasia is regularly fatal. 

In the severe cases the spasms are evidently painful and the strength 
of the patient is sapped by their recurrence. The spasms may spread 
to the face and involve even the respiratory muscles. There is no fever 
or constitutional disturbance, except such as belongs to the original 
disease or results from exhaustion. 

Diagnosis. — The spasms are easily recognized on sight. The vari- 



564 FUNCTIONAL NERVOUS DISEASES 



ous signs noted distinguish them from hysterical spasms. The primary 
rigidity of the neck and jaw with constitutional symptoms readily dis- 
tinguish true tetanus. 

Treatment.^ — The indicated treatment in these cases at present in- 
cludes the administration of preparations of the parathyroid glands and 
the salts of calcium. Preparations of the parathyroids are now offered 
by several manufacturers of glandular extracts. These preparations 
are not standardized and the dosage varies. Of the calcium salts the 
lactate is preferred. It may be given by the mouth, subcutaneously or 
intravenously. In a case of gastric tetany in an adult Kinnicutt gave 
intravenously 4 grams dissolved in 1,000 c.c. of normal salt solution 
daily for several successive days. An equal quantity can readily be 
given by mouth, when the stomach is tolerant. Hot baths may give tem- 
porary relief from the spasms. 

The underlying condition, rachitis, gastro-enteritis or gastric dilata- 
tion, must receive appropriate treatment. In gastric cases operation for 
the relief of pyloric stenosis causing dilatation must be considered, but 
is very likely to prove fatal because of exhaustion. 

OCCUPATION NEUROSES 
(Professional Spasms) 

Definition. — Irregular involuntary cramps of groups of muscles 
commonly employed in the repetition of certain acts peculiar to the 
occupation. 

Etiology. — Occupations requiring the continuous repetition of more 
or less complicated muscular movements, such as writing, telegraphing, 
typewriting, piano-playing and the like, are the essential cause. The 
affection, therefore, appears only in persons thus occupied. Practically 
every occupation which requires the continual repetition of certain 
muscular movements has its peculiar neurosis. The general condition, 
especially that of the nervous system, influences the development of the 
condition. Overwork, worry, excitement, fatigue from any cause favors 
it. Tuberculosis, diabetes, alcoholism, or any constitutional disease 
lowering the vitality of the patient predisposes to it. 

Symptoms. — These consist of cramps of the muscles or groups of 
muscles employed in the performance of the occupation, in most cases 
the muscles of the hand and arm, associated with more or less sensory 
disturbances. The condition is very closely akin to the cramps induced 
by over-fatigue. 

The difficulty develops very gradually as a rule, slowly increasing 
for months or years, before the patient seeks advice, but it may develop 
suddenly. On attempting the usual movements the muscles are thrown 
into spasms which render their action difficult, awkward and irregular, 
or even impossible. More or less pain accompanies each attempt, and 
the subject is ultimately forced to give up his occupation. The pain is 
often in the shoulder or elbow, rather than the hand. A fine tremor 



HYSTERIA 



565 



develops in the hand. Actual paralysis of muscles is seen only in ad- 
vanced conditions. 

Sensory disturbances are usually present. An unusual sense of 
fatigue or strain in the muscles involved is common. Anesthesia, hyper- 
esthesia or paresthesia may be present, but are uncommon. The elec- 
trical reactions are normal. Mental anxiety and depression are natural 
and are commonly marked. 

Course. — The affection tends to become chronic and incurable. The 
disability may vary with rest or improvement in the general condition. 

Treatment. — The general condition of the patient must be consid- 
ered, and the health improved by appropriate means. The use of alcohol 
and tobacco should be limited or stopped. Anemia or malnutrition 
should be appropriately treated. 

In milder cases a change in the method of working may be help- 
ful. Thus in writer's cramp, the free-arm movement in writing may 
be ta.ught, or the left hand substituted for the right. Sometimes the 
use of a very large pen-holder is an advantage. Similar measures may 
be employed in other callings. 

Massage, electricity, in various forms, hot and cold douching, or 
vibration may be employed locally. Active and passive exercise of the 
affected muscles in movements other than those in which cramp occurs 
is valuable. In many cases nothing but a complete change of occupation 
avails. 

HYSTERIA 

Definition. — Mobius defines it as a state in which ideas control the 
body and produce morbid changes in its functions. 

Etiology. — As the name suggests, the disease is much more frequent 
in women, but is not unknown in men. Puberty and adolesence are the 
favoring periods for its development, but the disease may appear in 
childhood, or continue to old age. Hysteria occurs in all countries and 
among all nations, but the Latin, Slav and Israelite are especially sus- 
ceptible. Heredity and education are the chief predisposing causes. 
The children of neuropathic parents are apt to inherit sensitive and 
unstable nervous systems. Faulty education often develops the emo- 
tional powers and fails to teach the necessity of self-control. The vic- 
tim of such conditions under any strain readily presents the phenomena 
of hysteria. The immediate cause of hysterical attacks is usually some 
mental or physical shock, thus sudden fright, grief, worry or trauma 
of any kind, or the debility produced by disease may directly precede 
the outbreak. Imitation has at all times played an important part in 
producing hysterical manifestations, especially in endemic and epidemic 
waves. Much of the demoniacal possession and of the witchcraft of 
ancient days is now recognized as hysteria. Schools, hospitals and 
religious gatherings have always been favorite fields for this disease. 

Symptoms. — These are best classified according to the French, who 
have devoted the most exhaustive study to the disease, into two great 
groups : ( 1 ) the stigmata, which are essentially persistent symptoms, and 



566 



FUXCTIOXAL NERVOUS DISEASES 



(2) the accidents, which are transitory. The stigmata of hysteria are 
sensory, motor and psychic. 

Sensory Stigmata. — (1) Anesthesia. This is most often confined 
to one side of the body, a hemianesthesia, but it may affect any part of 
the surface and the mucous membranes of the affected parts may be 
anesthetic. Except in the form of hemianesthesia, the hj^sterical affec- 
tion does not correspond to the distribution of any of the peripheral 
nerves or to areas supplied by any segment of the cord. Thus an anes- 
thesia appears in a single extremity, or as a band about the trunk or 
the limb, or in the form of a glove or stocking. The anesthetic zones 
are movable. Under the influence of suggestion employed by the appli- 
cation of metals, magnets, or the electrical current the area of anesthesia 
may be rapidly shifted from one part to another, or from one side of 
the body to the other. In some cases the elements of sensation are dis- 
associated and the anesthesia may be confined to loss of sense of pain 
or touch. It is characteristic of hysterical anesthesia that the patient 
is usually ignorant of this loss of sensory power until it is developed by 
examination. The loss of sensation may be associated with loss of 
motive power or may be entirely independent of it. The organic and 
tendon reflexes are not modified by hysterical anesthesia, as in organic 
lesions showing lack of sensation. The pupillary, abdominal, cremas- 
teric, knee and toe reflexes are preserved. 

(2) Hyperesthesia is very common. Headache referred to the ver- 
tex or occiput is frequent. The pain is often intense, and from its 
being compared to the driving of a nail into the head, has earned the 
classical designation of clavus hystericus. Pain in the back either 
localized or diffuse is an almost constant feature of hysteria. The hyper- 
sensitiveness may be confined to definite areas upon the trunk, espe- 
cially of the abdomen, and may therefore suggest disease of the under- 
lying viscera, such as the stomach, the appendix or the ovaries. Hyper- 
esthesia of the whole abdomen may be very suggestive of peritonitis. 
Pressure upon any hypersensitive point may promote an hysterical fit. 
Such points or areas are then spoken of as hysterogenic points or zones. 

]\IoTOR Stigmata. — Like the sensory stigmata, these are unknown to 
the patient, and must be elicited by examination. They differ only in 
degree from the motor accidents, from which, however, they should be 
clearly distinguished. (1) Movements in hysteria are retarded, the 
degree of retardation varA^ing as do the other symptoms. (2) Co- 
ordination is imperfect and movements are consequently awkward. (3) 
More than one movement at a time is usually impossible. (4) Volun- 
tary power as measured by the dynamometer is weakened. (5) There 
is a tendency to rigidity and contracture of various muscles. 

All of these motor stigmata are usually most marked in parts affected 
by anesthesia. The basis of these motor phenomena is the defective 
cerebral control of the patient, and they may be lessened by evoking 
active mental effort, or intensified by suggestion. 

Mental Stigmata. — The mental stigmata of the hysteric may be 



HYSTERIA 



567 



summarized as loss of will power and memory with an abnormal im- 
pressionability or susceptibility to suggestion. 

Suggestibility. — The mind of an hysterical person is abnormally sen- 
sitive to the slighest suggestion or impression, and an idea once ad- 
mitted, seems to develop to an extreme without any participation of the 
will or of the personal consciousness of the subject. This characteris- 
tic leads to imperfect and whimsical actions. 

Amnesia. — In the field of memory the consciousness of the hysteric 
undergoes a limitation analogous to the contraction of the visual field. 
In some instances the loss is slight, the memory of a person or place is 
lost, or again a complete group of sensory or motor images disappears. 
A hysteric may suffer from aphasia or agraphia, or may be unable to 
stand or walk (astasia-abasia) . In other instances the loss of memory 
may be almost complete, and the patient recalls only the facts and ideas 
closely associated with the mental state of the moment. From the in- 
teraction of this amnesia with the susceptibility to suggestion arise the 
phenomena of double or multiple personality which have been so fre- 
quently exploited with relation to hysterics. The defective memory is 
also the explanation of many of the charges of deceit or wilful lying 
made against these patients. 

Ahoulia. — (Loss of will-power.) From this spring vacillation, lack 
of initiative or enegy, and frequently inability to perform the slightest 
task. While these three elements, suggestibility, amnesia and aboulia, 
offer the best explanation psychology can present for the mental phe- 
nomena of hysteria, one must admit that they do not satisfy us. Partic- 
ularly do they fail to account satisfactorily for the behavior of many 
hysterical persons, whose apparently wilful simulation, deception and 
falsehood have led many physicians to emphasize their complete moral 
perversion. Certainly in dealing with them one must beware of being 
deceived or misled. 

Accidents. — The accidents of hysteria constitute the temporary or 
transitory phenomena of the disease. The accidents are the most strik- 
ing features of the condition, the symptoms which demand attention 
and most often bring the patient under the physician's observation. 
The most impressive of these accidents are the hysterical convulsive at- 
tacks. Of these major and minor forms may be described. 

Major Form. — The grand attack, as described by Charcot, consists of 
several phases. (1) A prodromal stage marked by mental depression or 
exhilaration sometimes accompanied by hallucinations. An aura fol- 
lows, usually a painful sensation rising from the abdomen to the throat, 
where it gives rise to a sensation of suffocation, the classic globus hys- 
tericus. (2) Convulsive stage. Closely resembling a true epileptic 
seizure with tonic and clonic convulsive movements. (3) Period of 
elownism, made up of a phase of contortions, followed by grand move- 
ments, such as flexion of the trunk or of the head. (4) Passional atti- 
tudes, expressive of fear, love, rage, etc. (5) Period of delirium with 
hallucinations. Visions are seen, voices heard, conversations held. After 



568 



FUNCTIONAL NERVOUS DISEASES 



a varying time the hallucinations fade and consciousness returns. At- 
tacks of such elaborate evolution are rarely seen in the United States. 
We are, however, familiar with the minor or modified attacks. 

Minor Attack. — This is regularly preceded by immoderate laughing 
or crying, and the globus hystericus may be felt. With these prodromata 
the patient passes suddenly into a convulsion of both tonic and clonic 
phases resembling the epileptic convulsion. In these seizures it is 
notable that the patient does not fall suddenly or in such a way as to 
injure himself or herself ; the tongue is not bitten, the urine is not passed 
involuntarily. The patient's movements are exaggerated and disorderly, 
so that upon the inexperienced the fit is always more impressive than a 
true epileptic attack. After a few minutes the convulsion usually sub- 
sides, the patient again becomes emotional and returns to consciousness 
or sinks into a torpid semi-conscious condition which lasts for hours, 
and from which he or she cannot be easily roused. 

Motor Accidents. — P aralyses . — These occur most often in the 
form of a paraplegia, but hemiplegia and monoplegia may be met with. 
The paralysis may be accompanied by anesthesia, or hyperesthesia, and 
may be as variable in degree as these symptoms. Vasomotor or trophic 
disturbance is rare, and tendon and electrical reactions are normal. 
Such paralyses may last days or years. 

Contractures . — These are closely related to the paralyses. 
They may be paraplegic, hemiplegic or monoplegic in type. The 
affected muscles are tense and hard, the part affected rigid, the con- 
tractures persist during sleep, but yield to complete anesthesia. Trophic 
disturbances are rare. Tendon and electrical reactions persist. They 
may be associated with disturbances of sensation. Rhythmic spasms 
are not uncommon in hysteria. There may be rhythmic movements of 
head, face, trunk or extremities, the movements repeated over and over 
for minutes or days. Tremors are also frequent, either alone or asso- 
ciated with other motor accidents. Any type of organic tremor may be 
reproduced by the hysterical affection. 

Cutaneous Accidents. — Eruptions of various kinds, edema, even gan- 
grene may occur. The phenomena of dermographism can usually be elicited. 
Hemorrhages from the skin and even bloody sweats are described. 

Cardiovascidar. — The heart action is usually normal, but may be 
greatly varied. Rapid heart action and palpitation may give rise to 
great distress. Slowing of the pulse is much less frequently seen. At- 
tacks of pain referred to the heart and associated with palpitation may 
closely simulate angina pectoris. 

Temperature. — Hysterical fever of various types and heights has 
been reported. As a rule the pulse and respiration do not correspond. 
Exceedingly high temperatures have been reported, 112° to 120° P., but 
suspicion, of course, always attaches to such cases, for no rational ex- 
planation of the observations has been given. 

Sensory Accidents. — Headache is often severe. It may be referred 
to the eye, to the vertex or the occiput. It usually comes in attacks in 



HYSTERIA 



569 



the afternoon or evening, and may be accompanied by nausea and vomit- 
ing. Tenderness over the spine is frequent, and may be so severe as 
to suggest disease of the vertebrte. Visceral neuralgias are common, 
and, as already observed, may suggest organic disease of abdominal 
organs. Hysterical angina pectoris is frequently met with. 

Visceral Accidents. — B espiratory . — Aphonia is a common 
complaint. Mutism is not so often seen. Hiccough, sighing, crying or 
talking, which may persist for long periods, are well known. Dyspnea, 
which may be very extreme, the respiration mounting to eighty or one 
hundred per minute, occurs. Any one of these respiratory disorders ap- 
pears alone or they may be associated with one another. They arise from 
sensory or motor disturbances in the respiratory muscles and organs. 

Digestive . — Anorexia nervosa is the most prominent of these 
affections. Food may be refused until an extreme emaciation or even 
death results. Spasms of the esophagus simulating stricture occur. 
Chronic vomiting may be of hysterical origin. Tympanites may develop 
and associated with spasm of abdominal muscles may simulate preg- 
nancy (pseudocyesis) or other forms of abdominal tumor. Hysterical 
peritonitis, that is, hysteria presenting the clinical picture of peritonitis, 
is well known. 

Urinary . — Reduction of the amount of urine is common, com- 
plete anuria for long periods possible also, although deception on the 
latter point must, be guarded against. Frequent urination and polyuria 
are also common, especially at the conclusion of the hysterical attack. 

Course and Prognosis. — Hysteria is essentially a chronic affection, 
lasting for months or years. The patient presents long periods of im- 
provement only under some unfavorable influence, such as undue emo- 
tion, or the exhaustion of acute disease to return to the old condition. 
On the other hand, the various accidents of hysteria, the affections 
which most often come under the physician's care, are usually readily 
relieved by appropriate medical treatment. There seems no doubt that 
hysteria while as a rule not dangerous to life may be fatal through some 
of its accidents, such as the anorexia and vomiting. 

Diagnosis. — The important point in this regard is to be on the look- 
out for hysteria, as there are few diseases, either acute or chronic, which 
may not be suggested by the phenomena of this disease. Hysterical 
affections have ear-marks, which, as a rule, readily identify them. The 
clinical picture is overdrawn or paradoxical. Thus the hysterical con- 
vulsion is a very exaggerated picture of the epileptic attack, and yet 
the condition of the patient afterward is very much better than in con- 
vulsions of organic origin. Anesthesia of hysteria never corresponds 
exactly to the territory of any nerve or any segment of a cord. The 
disability produced by hysterical paralysis is always much more marked 
than in an organic paralysis. The vomiting of hysteria is more severe 
than that produced by any gastric affection. The hyperesthesia of the 
abdomen may be more intense than that of an acute peritonitis, so 
that the suggestion of a touch leads to shrinking and complaint of pain. 



570 



FUNCTIONAL NERVOUS DISEASES 



This exaggeration of the clinical picture or contradiction between the 
sjTuptoms and the discernible lesion should always put one on guard. 
Then an investigation of the historj^ and careful examination of the 
patient for the stigmata of the disease will lead to a correct diagnosis. 
On the other hand, it must be remembered that hj^sterical patients may 
suffer from organic lesions which pass unnoticed in the presence of 
hysteria. Thus hysterical patients may easily develop tuberculosis or 
Bright 's disease which may be overlooked. 

Treatment. — From the nature of the malady, the treatment of hys- 
teria must be psychic. Suggestibility being so important a feature of 
the mental condition, an entire change of surroundings and companions 
is necessary. For this reason complete isolation of the patient is de- 
sirable. The visits of family or friends filled with s^Tnpathy and ready 
to discuss the patient's various complaints serve to maintain or even 
accentuate the perverted mental state. Having secured proper sur- 
roundings, the physician must seek to learn the exact mental state of the 
patient, especially to divine the controlling idea or ideas, and then 
to meet these by appropriate treatment. Thus the passage of a stom- 
ach tube by demonstrating the permeability of the esophagus may re- 
lieve difficulty in swallowing. Or by distracting the patient's attention 
one may be able to bend a previously rigid and powerless limb, and 
so convince the patient of the possibility of doing likewise. 

For the hysterical convulsion a sudden dash of cold water on the 
face and neck, a sharp command, a pressure upon a hysterogenic zone 
may bring relief. The common hospital practice of spraying the face 
and neck with a well-charged bottle of vichy or carbonic water is very 
effective. 

To meet the graver problems of the mental state underlying these 
accidents demands the utmost skill, tact and perseverance of the phy- 
sician. Progress can onl}^ be made as a rule by gradual education of 
the patient. For this purpose isolation and the rest cure of Weir 
Mitchell (see p. 579) have found general favor. But the rest cure can 
do little for these patients unless seconded by clear insight and the in- 
fluence of a strong mind. Weeks or months may be required for definite 
progress. Hypnotism may be of service in some cases, but its use is not 
unattended by danger, and of recent years has found less and less favor. 

Attention must be given to the nutrition and the general health. 
Anemia, constipation, etc., are to be treated appropriately. Sedatives, 
such as the bromides, valerian, asafetida, may be used in periods of 
special excitement or unrest, but altogether medicines have very little 
value except as called for by some definite symptom. They do not 
materially affect the underlying conditions. 

NEURASTHENIA 

Definition. — Neurasthenia is a functional nervous disorder depend- 
ent upon exhaustion of the central nervous system, and manifesting 
itself by sj^mptoms of either general or local weakness and irritability. 



NEURASTHENIA 



571 



Etiology. — Neurasthenia may be either hereditary or acquired. (1) 
Hereditary. Children of parents who either by reason of scant in- 
heritance or their manner of life have exhausted their store of nervous 
energy are liable to become the victims of neurasthenia. They have so 
small a stock of nervous energy to begin with that it may be readily 
exhausted. (2) Acquired. Neurasthenia is acquired by lack of proper 
relation between one's store of nervous energy and its expenditure. 
In normal life each day's damage to the nervous system is made good 
by the normal process of rest and repair. Whenever the drain becomes 
too great to be made good by these reparative processes nerv^ous ex- 
haustion or nervous bankruptcy must sooner or later result. Thus pro- 
longed excessive mental labor frequently leads to neurasthenia, and 
the disease is common among overworked business and professional 
men. On the other hand, neurasthenia may be seen following the ex- 
haustion of some of the acute infectious diseases, such as syphilis, 
typhoid fever and especially influenza. Finally, overindulgence in 
alcohol, tobacco, opium or cocaine may be the underlying cause for the 
development of neurasthenia. 

Inasmuch as the explanation of the disease is not infrequently a 
congenital lack of nerve force, it is not surprising that we at times 
meet with neurasthenia in children. It becomes much more frequent 
at the period of adolescence, especially in girls, when the normal de- 
mands of development as well as those of education put an unusual tax 
upon the nervous system. It is most frequently seen in mature life 
among men and women overborne by the cares of business or the worries 
of society. 

Symptoms. — The symptoms of neurasthenia are those of a slowly 
but steadily increasing exhaustion of either mind or bod}^, or both. In 
the beginning the patient finds himself more easily exhausted by either 
mental or physical effort. The day's work calls for greater exertion 
than usual. He is more nervous and more easily disturbed by the ordi- 
nary cares of life. As the process goes on he slowly but surely develops 
the full picture of nervous prostration. In its fully developed form 
the symptoms of neurasthenia may be classified as psychic, sensorj^, 
and motor or somatic. 

Psychic. — The psychic phenomena of neurasthenia are essentially 
those of brain fatigue. The patient can no longer carry on his simplest 
duties without an unusual degree of mental exhaustion. The most 
ordinary form of mental effort may become impossible. Reading, writ- 
ing, even ordinary conversation, may become too great a task for the 
weary brain. From this mental exhaustion of the brain, loss of will 
power, lack of initiative, inability to concentrate the attention, impair- 
ment of memory, and altogether a more or less complete failure of 
mental power result. Loss of the power of inhibition leads to an 
abnormal irritability. The ordinary trials of life affect the victim un- 
duly, and he frequently feels himself misjudged and ill-used. Anxiety 
is always a prominent feature of the mental horizon of the neuras- 



572 



FUNCTIONAL NERVOUS DISEASES 



thenic. He worries both about his affairs and his phj^sical condition. 
He is sure that some great disaster threatens him or that he is about 
to develop some deadly disease. In the extreme cases this anxiety of 
mind may become an abiding fear, producing the so-called phobias of 
the disease, such as agoraphobia or the fear of open spaces, or mono- 
phobia, fear of being alone, claustrophobia, the fear of being shut in, 
or as the climax of all, pantophobia, the fear of everything. The mind 
may be so harassed by fear and anxiety that suicide is not out of the 
question in these cases. 

Sensory Symptoms. — Headache is an almost constant concomitant 
of neurasthenia. The headache is regularly referred to the occiput, 
and is described in varying terms as a sense of oppression and con- 
striction or dull or sharp pain. The headache may be referred to any 
part of the head and may be described in various waj^s. Usually asso- 
ciated v/ith headache, there is a sense of lightness or fulness in the 
head, and vertigo of a more or less intense character is not infrequently 
met with. Pain in the back is regularly associated with the headache. 
This pain is most frequently felt in the lumbar region, but it may be 
referred to any part of the spine. With it there may be points of ten- 
derness scattered up and down the back over the spine, or under the 
angles of the scapulae. Pain and disturbances of sensation of any and 
all kinds may be met with in any part of the body. 

Pain may be complained of in any part of the body, and sensations 
of heat, cold, prickling, tingling, or numbness are common. On the other 
hand, anesthesia does not occur in uncomplicated neurasthenia. The 
most careful local examination fails to detect any adequate cause for 
the complaint of pain or disturbance of sensation. 

The Motor Symptoms. — The muscular weakness of neurasthenia is 
often pronounced. The most ordinary exertion, such as walking a few 
blocks, may produce profound fatigaie and complaint of pain. Effort 
that was formerly easy becomes impossible, the patient may even take 
to bed on account of physical disability. The underlying muscular 
fatigue may easily be demonstrated by asking the patient to repeat 
any voluntary muscular act, such as compressing the dynamometer. 
The action may at first be well executed, but each returning effort shows 
a rapid loss of muscular power. This myasthenia may be accompanied 
by tremor of the hand or face or local twitching. The tendon reflexes 
in neurasthenia are regularly increased, and a slight ankle-clonus may 
be demonstrated in some instances. Frequent repetition of these 
reflexes will, however, demonstrate the underlying muscular Aveakness 
by rapid exhaustion. 

Somatic Symptoms. — Neurasthenic patients often lose weight and 
become anemic. In the severest cases the malnutrition may be extreme. 
On the other hand, abundant adipose tissue and good color are not in- 
consistent with the diagnosis of neurasthenia. Apart from the general 
bodily disturbance, neurasthenia results in affections of individual 
organs, marked by excessive irritability, which is often characteristic. 



NEURASTHENIA 



573 



(a) Thus irritability of the retina or the muscles of the eye may give 
rise to painful sensations in the eyes and forbid prolonged use. Irri- 
tability of the retina may produce marked sensitiveness to light and 
even photophobia, (b) In like manner the auditory functions are dis- 
turbed, and there may be abnormal sensitiveness to noise of any kind, 
(e) Cardiac palpitation is one of the most common symptoms of neu- 
rasthenia, and often the cause of great discomfort. It is closely related 
to the digestive disturbances which belong to the disease, but may occur 
independently of them. Frequently there is associated with it a pain- 
ful throbbing of the arteries, most notably seen in the abdominal 
aorta, but extending even to the peripheral vessels, (e) More or less 
disturbance of the digestive functions regularly accompanies neuras- 
thenia, and in some instances this digestive disturbance may constitute 
the chief feature of the clinical picture. The patient complains of 
considerable discomfort after eating, and there is a more or less con- 
stant belching of air. Similarly the functions of the intestines are 
impaired, and constipation regularly accompanies the disease. Sexual 
disturbances frequently develop in the neurasthenia of men. They are 
distressed by nocturnal emissions or spermatorrhea, and suffer greatly 
from fear of impotence. 

Insomnia is one of the most constant symptoms of neurasthenia. 
There may be difficulty in getting to sleep or the patient after falling 
quietly asleep is disturbed by dreams, is restless, and awakes unre- 
freshed in the morning. 

One may find various types of neurasthenia described, such as cere- 
bral, spinal, gastric or sexual, depending on the prominence of symp- 
toms referred to these several parts, but neurasthenia is essentially a 
disease of the entire nervous organism with varying emphasis on symp- 
toms referred to special organs. 

Course. — The onset of neurasthenia is insidious, gradual. Once 
established the neurasthenic symptoms persist indefinitely unless inter- 
rupted by some radical change of life or proper treatment. The dis- 
ease may be protracted for years with varying periods of improve- 
ment and relapse. Patients who have once suffered from neurasthenia 
are liable to recurrence when subjected again to any unusual nervous 
strain. 

Diagnosis. — The picture of mental and physical weakness, com- 
bined with the impairment described in the functions of the various 
organs, is characteristic of neurasthenia. The essential feature of the 
disease is that of irritable weakness. There is no actual loss of power, 
such as is seen in a paralysis or contracture of organic origin. The 
most important part in the diagnosis of neurasthenia is to take care 
by thorough physical examination to exclude the possibility of organic 
disease, of which the neurasthenia may be purely symptomatic. 

Prognosis. — Neurasthenia is rarely or never fatal except from sui- 
cide. Recovery is the rule, if proper treatment can be instituted and 
carried out. The younger the patient the more likely he is to recover, 



574 



FUNCTIONAL NERVOUS DISEASES 



but the more liable be is to relapse. In patients over the age of forty 
the disease is very likely to become chronic. 

Treatment. — 'The prophylaxis of neurasthenia in childhood involves 
the adjustment of the life to the physical and mental constitution of the 
individual. The problems of diet, discipline, time of entering school, 
school hours, and school studies, rest, recreation and amusement must 
all be settled in such manner that, whatever the demands upon the 
nervous system of the child, they shall not only be met, there shall be 
laid up a store of nervous energy for use in later years. There is no 
cjuestion that many children suffer from defective management in this 
respect. The long hours at school with the hea^^^ tasks at home often 
work serious harm. Far too many children during their school careers 
present manifest evidences of neurasthenia, or at its close are so sapped 
of nervous energy that they have no store left to meet the demands 
of later life. The prevention of such results should be part of the duty 
of evers^ family physician. The prophylaxis of neurasthenia in mid- 
dle life calls for exactly the same adjustment of the nervous energy of 
the patient to the demands made upon it. At this time we must take 
into consideration the nature of the occupation, the amount of time 
devoted to it, the manner of life, the question of rest or recreation and 
amusement, every phase of life calling for the expenditure of nervous 
or physical energy, and the means of restoring them. Inasmuch as at 
this period the disease is essentially a fatigue neurosis, the vital point 
in its treatment is to secure rest for the nervous system. In the milder 
cases a temporary reduction of work, combined with exercise in the open 
air, and freedom from care, may be all that is required. In other cases 
a good vacation in the woods or a trip abroad may enable the patient- 
to regain his lost nerve force. In the severer type of the disease, how- 
ever, adequate treatment requires months of time, and taxes the skill 
of the most resourceful physician. The patient often requires physical 
as well as mental rest, and isolation is necessary. For such patients 
the rest cure of AYeir ^Mitchell has proved the most satisfactory method 
of treatment. In addition to isolation, rest in bed, overfeeding, massage 
or electricity are used, all for the purpose of restoring nerve and mus- 
cle tone, or for suggestive impression. The general features of this 
method are presented in the following details of the daily program : 

Seven a.m., cocoa, followed by a cool sponge bath with a rough rub, 
and the toilet for the day. 8 a.m., breakfast with milk. Eest an hour 
after. 10 a.m., 8 ounces of peptonized milk or its equivalent. 12 m., 
8 ounces of milk or soup, after which the patient can be read to by the 
nurse. 1.30 p.m., dinner, followed by rest for an hour. 3.30 p.m.. 8 
ounces of milk and a half hour later the application of electricity. 6.30 
p.m., supper with milk, followed by rest for an hour, after which the 
patient may be read to for half an hour or longer, if it does not fatigue 
him or her. 8.30 p.m., administration of malt extract with an aperient, if 
necessary, or the utilization of some measure of treatment for insomnia, 
such as the drip sheet, or the administration of an hypnotic. Valuable 



TRAUMATIC NEUROSES 



575 



as this method is in itself, it will succeed only when backed by the 
constant service of an intelligent nurse and the influence of a physician 
who has faith in it, and who enjoys the confidence of his patient. Un- 
der the treatment patients regularly gain rapidly in weight and in 
nervous tone. The treatment must be carried out for weeks or months, 
depending upon the severity of the case, and the progress made toward 
recovery. 

The relief of local sources of irritation is not infrequently an im- 
portant part of treatment. Thus the wearing of proper glasses for the 
relief of eye-strain may be an essential element of the cure. Similarly 
the proper treatment of uterine or ovarian disease may in some cases 
be very important, but radical operations upon neurasthenics are to be 
avoided as long as possible. Finally alcoholism or drug habits must be 
treated by appropriate measures. 

In other and milder cases, especially in men, systematic physical 
exercise in the open air is of great value. In the early stages an hour's 
work in a gymnasium daily, or every other day, allays the disturbance 
and permits continuance of work. In severe conditions weeks or months 
must be given up to systematic physical culture under ideal conditions. 

Physical culture to be most effective must be combined with com- 
plete relief from mental labor or anxiety, and with such diversions as 
employ the time and lead to entire peace of mind. 

Hydrotherapy is of very great value. Spinal douches, cold packs, 
or cold shower baths, etc., must be employed according to the patient's 
condition. Massage is invaluable for the relief of the general physical 
exhaustion or for local irritability. 

Electricity is often employed for its sedative effect upon the spinal 
centers especially, and the various forms of electric current, high fre- 
quency, sinusoidal and the Roentgen rays, are employed for the purpose. 
Various sanatoria and health resorts employing some or all of these meas- 
ures offer the most effective treatment for these patients. 

TRAUMATIC NEUROSES 
(Traumatic Neurasthenia or Hysteria) 

Definition. — A condition of neurasthenia or hysteria developed as a 
consequence of the physical or psychic effect of accident or injury. 

Etiology. — Any mental shock may be followed by the development 
of neurasthenia or hysteria. Physical injury increases the probability 
of such a result. Neurasthenia or hysteria therefore frequently follows 
accidental injuries sustained in railroad accidents, fires, explosions and 
the like. They may, however, follow when no injury has been re- 
ceived, merely from the mental shock. The possibility of recovering 
damages often intensifies the effects of the experience. 

Morbid Anatomy. — Many theories have been advanced as to the 
nature of the changes underlying these conditions, but none of them has 
been satisfactorily demonstrated. 

I 



576 



FUNCTIONAL NERVOUS DISEASES 



Symptoms. — The clinical picture is that of neurasthenia or hys- 
teria, or a combination of the two. It may include any of the usual 
symptoms of these disorders, even in their severest forms. Pains of 
various kinds and locations, tingling, numbness, formication and the 
like, and loss of power, complete or partial, hemiplegic, paraplegic or 
monoplegic in type, are common complaints. Mental power, speech and 
the special senses may suffer in an endless variety of ways. 

Course and Prognosis. — The conditions usually improve slowly, 
and health is ultimately regained. Recovery is often prompt after de- 
cision of damage suits, because of the mental relief, and quite inde- 
pendently of the question of malingering. In some cases the condi- 
tion becomes chronic and persists indefinitely. 

Diagnosis. — Careful investigation of the history of the patient and 
careful physical examination are essential. Previous organic disease 
may be excluded by these means, for it must be remembered that 
patients having organic disease may present hysterical symptoms. Ma- 
lingering must be borne in mind and the patient subjected to various 
tests to bring out the sincerity of his complaints. Thus spots reported 
exceedingly painful and tender may be freely pressed, if the patient's 
attention is diverted by conversation, or the reflexes of a supposedly 
paralyzed limb found to be normal. Hoover 's test for hysterical paraly- 
sis of the leg is of interest. In organic hemiplegia, if the patient lying 
supine attempts to raise the paralyzed leg the heel of the normal side 
is pressed downward — i.e., into the bed. In hysteria or malingering 
no such action would occur. 

Treatment. — ^The treatment must be that of neurasthenia or hysteria. 

PERIODIC PARALYSIS 
(Family Periodic Paralysis) 

Definition. — A flaccid paralysis of the muscles of the trunk or ex- 
tremities, temporary and recurrent at fairly regular intervals. 

Etiology. — The disease appears in certain families, in one recorded 
instance affecting four successive generations. The transmission is .by 
either male or female branch. Cases have been recorded as early as the 
fifth year, but the onset may be delayed till after thirty. The patholog}^ 
of the disease is not established. A certain resemblance to myasthenia 
gravis is noted. 

Symptoms. — Over night, the patient, previously well, develops a 
flaccid paralysis of all extremities, and possiblj^ of the trunk. The re- 
flexes are lost. In some instances even the muscles of the face and 
tongue have been affected. 

The paralysis lasts hours or days, and then gradually disappears. 
Milder and abortive attacks may be observed. The attacks recur from 
time to time without apparent cause. The severity of the attacks dimin- 
ishes later in life and death is rare. Treatment must be directed to the 
maintenance of normal physical and mental tone. The systematic ad- 
miiiistratioii of the bromides is advised. 



RAYNAUD'S DISEASE 



577 



ASTASIA-ABASIA 

These terms denote a certain symptom-complex met with in various 
conditions, especially hysteria, epilepsy, chorea and the like. Although 
muscular power, sensation and coordination are normal, so that lying 
in bed power and motion are normal, the patient is unable to stand 
(astasia) or to walk (abasia). Most cases show no spasm, rigidity or 
ataxia; in others there are spasms and irregular jerky movements. The 
treatment must be directed to the underlying condition. 

RAYNAUD'S DISEASE 

Definition. — A vasomotor affection, showing no organic lesions, in 
which localized anemia or congestion leads to disturbance of function 
or rarely to necrosis of the part involved. 

Etiology. — The disease is rare. In many cases no explanation is to 
be found. In others a hereditary or family neurotic constitution is 
accused. Sudden fright or shock may precede the attacks. Women are 
attacked more frequently than men, and cases in children have been 
recorded. Exposure to intense cold is often given as the cause of 
attacks. 

Morbid Anatomy. — Theory has attributed the condition to spasm 
or paresis of the vaso-constrictors in the affected part. Peripheral 
neuritis has been found in some cases; endarteritis obliterans in others, 
but these cases with definite organic lesions should, for the present, be 
excluded from this category. 

Symptoms. — Three stages of the disease are described, in any^ one 
of which the patient may first be observed. 

1. Stage of local syncope. Following exposure to cold, mental 
shock or excitement or gastric disturbance, one or more -fingers or toes 
or the whole hand or foot becomes white, cold, and numb. This condition 
persists for a few hours, and then the circulation returns to normal 
or passes into the second stage. 

2. Stage of asphyxia. The affected part or parts become livid, mot- 
tled, deep red or purple. Intense pain or anesthesia may be complained 
of. The parts may appear swollen and puffy. Like the first stage this 
condition persists for some time, and then gradually gives place to the 
normal. The affection is frequently symmetrical on hands or feet. In 
most cases the attacks are repeated from time to time, either with or 
\\'ithout definite cause. 

Constitutional symptoms are ordinarily lacking, but hemoglobinuria 
has been observed in some patients, as though hemolysis had occurred, 
and in others temporary visual disturbances, mental dulness, hemi- 
plegia or aphasia during the attacks have suggested that vascular dis- 
turbances similar to those in the extremities were taking place in the 
eye or the brain. 

3. Stage of gangrene. Occasionally a dry gangrene follows the 
cyanotic stage. The affected finger or toe becomes dry, shrivelled, dead ; 
a line of demarcation forms in time and the dead portion sloughs away. 

37 



578 



FUXCTIOXAL NERVOUS DISEASES 



Slow cicatrization follows. A hand or leg may be lost in sLiccessive 
attacks. The ears or nose may also be inYolved in severe cases. 

Diagnosis. — The phenomena of Raynaud's disease are easily recog- 
nized. The propriety of the diagnosis depends npon the careful exclu- 
sion of definite organic disease. Error is easy in patients seen only 
once. The recurrence of the phenomena is highly suggestive of Ray- 
naud's disease. 

Diabetes, embolism or thrombosis of the vessels of the affected part, 
disease of the spinal cord, such as tabes or syringomyelia, multiple 
neuritis (beri-beri) and ergot-poisoning must be excluded by care in 
the examination of the patient. Of late the studies of Buerger and 
others have laid emphasis, especially in elderly patients (Hebrews), 
upon the presence of a definite obliterating thrombosis in the arteries 
of the affected extremity. 

Treatment. — The general health of the patient must be maintained 
on as high a level as possible. If cold causes attacks, residence in a warm 
climate during the winter is advised. Hydrotherapy, local massage, and 
electricity, either galvanism or the high frequency current, have been 
of service. 

During the attacks pain may be relieved by bathing in hot water, 
or the hot-air bath. Bier's method may be tried, if other measures fail. 
In severe cases morphine may be required. If gangrene develops, the 
part must be kept as nearly- aseptic as possible. Amputation may in the 
end be necessary. 

ERYTHROMELALGIA 
(Red Neuralgia) 

Definition.— A rare chronic vasomotor affection in which congestion, 
pain and local heat develop in some part or parts of the body, especially 
in the extremities, when they are dependent. 

Etiology. — Men are more often affected than women. Exposure, 
overexertion and sudden strain have been considered as possible causes. 
The condition is regarded as a vasomotor neurosis closely related to 
Raynaud's disease. 

Morbid Anatomy. — Local lesions of the arteries, or the nerves, or 
the posterior spinal nerve-roots have been found, but the pathology 
is not yet established. A localized neuritis or endarteritis would explain 
the conditions. 

Symptoms. — Redness, pain and swelling develop in the aft'ected 
part, most often a foot or hand, especially following use. The aft'ection 
may be symmetrical. Standing or walking intensifies the disturbance. 
The condition is more or less chronic, but may disappear. 

Diagnosis. — As in Raynaud's disease careful examination must be 
made for organic disease. From Raynaud's disease the affection is dis- 
tinguished by its prevalence in women, the absence of any stage of 
anemia, the increase of sjmiptoms when the part hangs down, or on ex- 
posure to heat (summer), the higher temperature of the aft'ected parts, 



FACIAL HEMIATROPHY 



579 



and the absence of gangrene. In some cases the distinction is extremely 
difficult. 

Treatment must be along the lines indicated under Raynaud's dis- 
ease. Cold rather than heat gives relief to pain. Rest is important. 
Excision of the nerves of the affected part has been helpful. 

FACIAL HEMLITROPHY 

Definition. — A slowly progressive atrophy of the bones and soft tis- 
sues of one side of the face. 

Etiology. — About 200 cases of this rare affection are recorded. The 
patients are usually women. The cause is not known. At autopsy an 
interstitial neuritis of the fifth nerve has been demonstrated. The cer- 
vical sympathetic may also be involved. 

Symptoms. — AVhitish patches (leukoma) appear on the skin of the 
face. Skin and subcutaneous tissue atrophy till the skin appears to 
rest upon the bone. The hair and eyebrows may fall out or become 
white. The eyeball may sink, owing to disappearance of the orbital fat. 
The tongue may show hemiatrophy. Even the bones atrophy and the 
teeth may fall out. The result is a very great disparity in the two sides 
of the face. Various sensory disturbances may accompany the atrophy. 

Treatment is unavailing. 

ANGIONEUROTIC EDEMA 
(Quincke's Disease) 

Definition. — A neurosis characterized by the development of areas 
of acute edema of the skin or mucous niembranes. 

Etiology. — Young adults are most often affected. Like other 
neuroses the tendency appears to be hereditary in some families in Avhich 
other neuroses are known. Theoretically the condition results from a 
localized vasomotor disturbance. It closely resembles urticaria and 
may be related to the skin reactions produced by the infection of anti- 
toxic and other sera, the so-called anaphylaxis. 

Symptoms. — Sharply localized areas of soft, puffy swelling develop 
on the face, especially the eyebrows, ears or lips, on the hands or feet, 
or on the tongue, throat or genitalia. The swellings are dift'use, smooth, 
not tender or painful, pale or slightly flushed. There are no constitu- 
tional symptoms. The swellings last a few days, then disappear, to 
recur from time to time, at irregular intervals. 

In a few cases constitutional symptoms, headache, fever, and somno- 
lence, accompany the edema. 

In patients whose gastro-intestinal mucous membrane is involved, 
severe attacks of abdominal pain, vomiting and prostration may occur. 
Death has resulted from such attacks or from acute edema of the larynx 
of angioneurotic origin. In such visceral attacks the affection is closely 
akin to Henoch's purpura, the lesions being edema instead of hemor- 
rhages. 



580 



FUNCTIONAL NERVOUS DISEASES 



Treatment. — The general health must be improved by attention to 
diet, exercise, rest and hygiene. Articles of diet found to produce 
attacks must be excluded. The administration of calcium lactate, 20 
grains, thrice daily, may be helpful. 

SCLERODERMA 

Definition. — A diffuse or patchy induration of the skin sometimes 
followed by atrophy, apparently a trophoneurosis. 

Etiology. — The patients are commonly between 20 and 40 years of, 
age; two-thirds of the cases recorded have been in women. The affec- 
tion may follow an acute infectious disease, but there is no satisfactory 
etiology. 

Morbid Anatomy. — Endarteritis of the vessels of the affected area 
with hypertrophy of the several parts of the skin, but especially the 
connective tissue, has been found in most cases examined. 

Symptoms. — The face and extremities are the most common seats 
of the affection. The affection may remain localized (morphea) or 
may extend to the skin of the whole body. 

A white marble-like induration of the skin is usually the earliest 
symptom. On the affected area the skin cannot be picked up in the 
usual fold. It indents but slightly, if at all, on pressure. More or less 
stiffness of the affected part results. Atrophy of the skin gradually 
follows, and it then becomes dry, parchment like, and adherent to the 
underlying tissues. Areas of deeper pigmentation (brownish) and 
patches of leukoderma are found in the atrophic areas. An eiythema 
or cyanosis of the affected skin is sometimes observed, particularly in the 
hands or feet, giving the affection a close resemblance to Raynaud's 
disease. Trophic disturbances, such as paronychia, ulceration, and loss 
of hair, may occur in the skin itself, and in the underlying parts an 
atrophy of both muscle and bone has been observed. Constitutional 
symptoms, such as fever and diarrhea, have been recorded, but are rare. 

Course and Prognosis. — The disease may run a rapid or a chronic 
course. Some cases recover, many die of exhaustion. 

Diagnosis. — The affection is usually easily recognized. Raynaud's 
disease is suggested by some cases, leprosy by others. Myxedema must 
also be considered. 

Treatment. — The Continued administration of the thyroid extract 
has seemed to help some cases. Many other drugs have been tried but 
without result. Hydrotherapy, especially as carried out at various min- 
eral springs, the local application of the Roentgen rays, massage and 
electricity are recommended. 

ACROMEGALY 

Definition. — A rare chronic disease marked by progressive increase 
in the size of the bones of the head and extremities, and related to morbid 
function of the pituitaiy gland. 



ACROMEGALY 



581 



Etiology. — The disease develops in the third decade. People of 
large size are especially subject to it, but dwarfs are not immune. No 
satisfactory cause is known. 

Morbid Anatomy. — All the bones of the body, but especially those 
of the extremities, are enlarged. The increase is due to subperiosteal 
growth. All prominences, ridges, or grooves are accentuated. The 
outer table may be increased in density. Exostoses are common. The 
pituitary gland is often enlarged, especially the anterior lobe. The en- 
largement may be of any pathological type, simple hypertrophy, a cyst, 
or a malignant growth. Enlargement of some of the thoracic organs 
has also been observed. 

Symptoms. — The patients complain of headache, irritability, loss of 
memory, pains in various parts of the body, constipation, and polyuria. 
On examination the characteristic overgrowth of the head, the nose, 
the jaws and the extremities is found. The larynx is often enlarged 
and the voice is deeper than normal. The spine shows various deformi- 
ties, kyphosis, scoliosis, or curvatures. The hands and feet may be enor- 
mous. All parts of the body, orbit, ears, heart, liver, and spleen may 
show enlargement. 

The muscles are not affected and reflexes are normal. An unlimited 
variety of disturbances of the functions of the body has been recorded 
in various cases. 

Acromegaly often presents some of the symptoms of exophthalmic 
goitre, syringomyelia, myxedema or epilepsy. 

The course of the disease is variable. Remissions occur and the 
course is very chronic, lasting even fifty years. Malignant cases with 
very rapid enlargement are rare. A cachexia finally develops and the 
patients die of exhaustion or from the dilatation and failure of the 
heart. 

Diagnosis.- -In typical or advanced cases the diagnosis is easy. In 
early stages the enlargement of the extremities may be overlooked and 
the disease mistaken by reason of the variety of associated symptoms. 
Skiagraphs of the bones of the head and extremity are important. En- 
largement of all these parts belongs only to acromegaly. Pulmonary 
osteo-arthropathy gives a history of pulmonary disorder and no involve- 
ment of the face, and no nervous symptoms. Gigantism presents no dis- 
proportionate enlargement of the bones. Arthritis deformans and 
osteitis deformans may be suggested, but are readily excluded by care- 
ful examination. 

Treatment. — Pituitary therapy has thus far been without value. If 
a definite tumor of the pituitar^^ can be made out, surgical removal may 
be attempted. Otherwise treatment must be wholly symptomatic. 



APPENDIX 



THE GENERAL CARE OF THE SICK 

The adequate treatment of the sick involves much more than the 
prescription of medicines. In many of the conditions with which we 
have to deal the welfare of the patient depends more upon the general 
regime, rest, careful feeding, regular evacuation of the bowels, and sleep, 
than upon the medicines administered. A^-hile these general subjects 
have been mentioned in the discussion of the treatment of diseases 
already given, certain details require separate presentation. 

Choice of the Sick-room. — In most instances other considerations 
than choice determine the question of the character of the sick-room. 
Where choice is possible the room should be large, at least 1,000 cubic 
feet in capacity, and should have abundance of sunshine and fresh air. 
In certain conditions, such as meningitis or measles, it may be necessary 
to darken the room, but under ordinary conditions both light and air are 
to be freely admitted. The light should, however, never fall directly 
into the eyes of the patient. 

Ventilation. — For many years all attempts to ventilate sick-rooms 
or hospitals were based upon calculations of the amount of carbon 
dioxide given off by one person and the atmospheric content of this gas 
consistent with comfort and health. Thus it was calculated that an 
individual exhales 14.4 cubic feet of carbon dioxide in 24 hours, and 
that the proportion of this gas in the air should not exceed six parts in 
10,000. To meet these conditions it was established that each individual 
requires 3,000 cubic feet of fresh air per hour. On this basis many 
different systems of ventilation for homes and hospitals have been de- 
vised, but none of them has proven equal to the free ventilation secured 
by opening windows wide or placing the sick on balconies or roofs, or 
entirely in the open air. The success attending the open-air treatment 
of the tuberculous has led to the adoption of the method, modified to 
meet different conditions, in the treatment of most of the disorders in- 
cluded ^dthin the sphere of internal medicine. The most satisfactory 
method in hospitals consists in having balconies in direct connection with 
the wards, so that the beds mounted on casters may be wheeled into the 
open air. For purposes of treatment requiring the exposure of the body 
of the patient, the bed is taken into the ward. Experience with this 
method has proven that so long as the body and especially the extremi- 
ties are kept warm, even the feeblest patients are invigorated by breath- 
ing cold fresh air. Draughts have been shown to be harmless, if the 
head be protected by cap or hood. Thus protected, even patients suf- 
fering from pneumonia may lie in the draught of an open window with 
positive advantage. Chilling of the surface of the body should at all 
times be avoided by adequate bed-covers or clothing, especially in 
582 



GENERAL CARE OF THE SICK 



583 



patients suffering from circulatory disorders with heightened blood 
pressure, since the contraction of the peripheral vessels by cold may in- 
crease the pressure. In the feeble the condition of the feet should be 
constantly Avatched, and, if they tend to become cold, artificial heat 
should be applied, usually by the use of the hot-water bottle. So long 
as the external atmosphere is cold, the hands and arms should be kept 
under cover. If this is impossible, on account of restlessness or delirium, 
they should be protected by capes and mitts. 

In private houses it is ordinarily necessary to close and warm the 
sick-room for baths or any other treatment requiring the exposure of 
the body, since the difficulty of moving the patient from one room to 
another is too great. 

In applying these teachings it must be borne in mind that they are 
radically opposed to many deep-rooted convictions of the layman. The 
fear of fresh air, and especially of draughts, is still common, and only 
by judicious management can the physician who attempts to carry out 
the open-air treatment of his patients escape criticism or censure for 
developments not justly chargeable to the method. 

Cleaning the Sick-room. — Whenever practicable the patient should 
be removed to another room. In any event the room should be cleaned 
and dusted in such a manner that dirt and dust will be gathered up, not 
scattered abroad. For this purpose vacuum cleaning is ideal. Sweep- 
ing should be done with a broom covered by a moistened cloth, and the 
dusting-cloths should likewise be moist. 

Isolation in Contagious Diseases. — In the treatment of contagious 
diseases, measles, scarlet fever, diphtheria, small-pox, German measles, 
chicken-pox, etc., special care is necessary to prevent the spread of the 
infection. The regulations of the New York Board of Health for the 
isolation of cases of measles, scarlet fever or diphtheria are here given: 
1. Complete isloation of every case of diphtheria as ordered by the medi- 
cal inspector of the Department of Health must be maintained until 
the disease is at an end and fumigation has been performed. 2. Chil- 
dren in the family must not be allowed to attend school until they have 
received a certificate from the Department of Health. 3. The room 
used for the case should be as nearly bare of furniture as possible. Car- 
pets and hangings should be removed before the patient is placed in 
the room. Toys or books used by the sick person should be thoroughly 
disinfected or destroyed after recovery or death. The sick-room should 
be well aired several times daily, the floor mopped and woodwork fre- 
quently wiped with damp cloths. Under no circumstances must the 
floor be swept when it is dry. It should be sprinkled with sawdust, 
bits of newspaper or tea leaves, all thoroughly moistened, and then 
carefully swept so that no dust may arise. 4. When practicable, one 
attendant should take entire care of the patient, and no one else beside 
the physician should be allowed in the room. The attendant should have 
no communication with the rest of the family. Visitors must not be ad- 



584 



APPENDIX 



mitted to the apartment as long as the placard remains on the door. 5. 
Plates, cups, glasses, knives, forks, spoons, etc., used by the patient 
should be kept for his especial use, and under no circumstances removed 
from the room or mixed with similar utensils used by others. They 
should be washed in the room in hot soap-suds, and then rinsed in boil- 
ing water. After use the soap-suds should be thrown into the water 
closet. 6. All cloths, bed linen and personal clothing which have come 
in contact in any way with the patient should be immediately immersed 
in a 21/^% carbolic solution before removal from the room. They 
should be soaked for one hour and may then be removed from the room 
and boiled in water and soap-suds for five minutes. 7. Surfaces of any 
kind soiled with discharges should be immediately washed with the car- 
bolic solution. 8. The discharges from the nose and mouth of the 
patient should be received on handkerchiefs or cloths, which should be 
at once burned or immersed in a 2i/^% carbolic solution. 9. After mak- 
ing applications to the throat or nose of the patient, and before eating, 
the hands of the attendant should be disinfected by scrubbing in hot 
soap-suds. 10. When the skin of the patient is peeling, the body should 
be washed daily with warm soap-suds and afterwards anointed with oil 
or vaseline. This should be repeated until all roughness of the skin has 
disappeared. 11. After the inspector of the Department of Health has 
ordered fumigation, the entire body of the patient should be bathed and 
the hair washed with hot soap-suds. The patient should then be dressed 
in clean clothes (which have not been in the sick-room during the illness) 
and removed from the room. The attendant should also take a bath 
and put on clean clothes before mingling with the family or other peo- 
ple. The clothes worn in the sick-room should be left there to be fumi- 
gated with the room and its contents. Under no circumstances should 
the sick-room be again entered or occupied or anything removed from 
it until fumigation has been performed. 

In the milder contagious diseases, such as chicken-pox, German 
measles, whooping-cough, the isolation is less rigidly practiced, but 
always with some risk to others. 

The source of contagion in cholera, dysentery and typhoid fever 
being limited to the feces and urine, the spread of the contagion can be 
prevented without isolation, but cholera patients, on account of the fear 
of the disease, are usually isolated, and isolation of typhoid fever 
patients has been repeatedly urged. Visitors or others coming in con- 
tact with the bed clothing of such patients are certainly exposed to dan- 
ger of infection. 

It would hardly seem necessary to forbid the kissing or fondling of 
patients sick with contagious diseases, but experience teaches the need 
of constant repetition of such prohibition. 

Disinfection. — The room or rooms occupied by a person suffering 
from contagious disease should be disinfected. This is usually required 
by Boards of Health after small-pox, measles, scarlet fever, diphtheria^ 



GENERAL CARE OF THE SICK 



585 



cholera, the plague, typhus, typhoid fever and tuberculosis. It is de- 
sirable after the milder affections, such as chicken-pox, German measles 
and whooping-cough. 

In every case of disinfection in New York City the following regu- 
lations must be complied with: 

All cracks or crevices in rooms to be disinfected must be sealed or 
calked, to prevent the escape of the disinfectant. 

The following disinfectants may be used in the quantities named: 

Sulphur, 4 lbs. for every 1,000 cubic feet, 8 hours' exposure. 

Formalin, 6 oz. for every 1,000 cubic feet, 4 hours' exposure. 

Paraform, 1 gr. to ewery cubic foot, 6 hoars' exposure. 

After fumigation for diphtheria or scarlet fever, bedding, carpets, 
rugs, etc., will be removed for sterilization. For this purpose formalde- 
hyde and steam under pressure are employed. 

All glass or earthenware dishes or vessels used about the patient 
should be soaked for several hours in 5% carbolic or 1/1000 bichloride 
solution. Metallic objects should be treated with carbolic. The wood- 
work should be wiped with the carbolic solution and the walls should 
be freshly papered or painted. 

General Care of the Patient. — The Skin. — A daily cleansing bath 
is desirable. If the patient's condition permit, he may be allowed to 
tal^e an ordinary tub-bath. If he is confined to the bed, a sponge-bath 
may be given by a nurse or attendant. After such a bath it is the com- 
mon practice to rub the body, but especially the back, with alcohol, and 
follow^ this with a simple dusting powder of talcum or boracic acid. 
This use of alcohol and powder must be repeated several times during 
the day in the seriously sick. It is not only grateful to the patient but 
serves to prevent the furuncles, abscesses or bed sores which so often 
develop in the bed-ridden, especially in those suffering from lesions of 
the nervous system attended by paralysis or loss of sensation. 

The development of bed sores, which are largely due to the influ- 
ence of pressure upon tissues w^hose vitality is lowered by exhausting 
disease, may be further guarded against by frequent changes in the 
position of the patient, the judicious use of pillows, air-rings and like 
devices for taking the pressure off threatened areas. If bed sores 
develop, they must be relieved of pressure, cleansed antiseptically and 
dressed with some stimulating application, such as balsam peru and 
castor oil, equal parts, or a dry powder of boric acid or other antisep- 
tic. Watchfulness is necessary to detect collections of pus about or 
leading from a bed sore, and by early incision limit the extension of 
such processes. In any case of protracted illness when bed sores 
threaten, an air- or water-bed is advisable. 

The Eyes. — The bed should be so placed that the light does not fall 
directly in the patient's eyes. If necessary, an eye-shield may be em- 
ployed, or the face shaded by a screen. Only under rare conditions, 
such as acute meningitis or tetanus, or in diseases accompanied by acute 



586 



APPENDIX 



inflammations of the eyes, should the room be continuously darkened. 
On the other hand, darkening the room for an hour after the mid-day 
meal is most helpful in enabling a patient to get a nap at that time. 

The Mouth. — In all fever patients and in those too feeble or indiffer- 
ent to care for themselves, the mouth must be given special attention. 
Such patients regularly breathe through the mouth, the mucous mem- 
brane becomes dry, brown, fissured, and perhaps eroded, the tongue and 
teeth are covered by an accumulation of food, desquamated epithelium, 
bacteria, and in severe cases, blood. Feeding is interfered with by pain 
and the mouth becomes a source of infection to the adjacent glands and 
tissues, and possibly of systemic infection. 

In these cases, therefore, the mouth must be cleansed after each feed- 
ing, either by rinsing with an antiseptic solution, such as the liquor 
antisepticus or liquor antisepticus alkalinus of the National Formulary. 
When the patient cannot do this for himself, the mouth should be 
cleansed by the nurse. For this purpose cotton may be wrapped on bits 
of wood or upon the nurse 's finger, and by these means the solution may 
be carried to all parts of the mouth. 

If the parts become dry, they, may after washing be anointed with 
albolene or Avhite vaseline. 

The Hands. — Attention to the condition of the hands is very neces- 
sary in the severely sick, especially in typhoid fever and other diarrheal 
conditions. The possibility of reinfections from the hands must be borne 
in mind, and care taken to prevent them. In delirious patients it may 
be necessary to tie the hands to the sides of the bed to prevent constant 
picking at the lips or nose. 

The Feet. — Coldness of the extremities adds greatly to discomfort 
and vital depression. In the seriously sick or very feeble the condition 
of the feet should be constantly watched and their warmth maintained 
by sufficient covers or the use of the hot-Avater bottle. 

Enemata. — 1. Cleansing. — For this purpose water at 100° F. con- ■ 
taining sufficient castile or other mildly irritating soap (not laundrj^ 
soap) to make it turbid is employed. For an adult from one to two 
quarts are ordinarily given. The patient should lie upon his back, with 
the hips elevated on a douche pan, but if this position is distressing, the 
injection can be given with the patient sitting up. The fluid to be 
injected is suspended in a douche-bag not more than three feet above the 
level of the body. The ordinary hard-rubber douche nozzle may be 
employed, but the soft rectal tube is preferable. In introducing the 
rectal tube care must always be taken to prevent its doubling upon 
itself in the rectum. After the tip has been inserted its advance is fav- 
ored by allowing a little of the fluid to enter in advance of the tube. 
(2) Milk and molasses in equal parts have been found to make a very 
satisfactory cleansing enema. About eight ounces of the mixture are 
usually required. The relatively small quantity is in some patients 
an advantage. (3) For the relief of abdominal distention and tympan- 



GENERAL CARE OF THE SICK 



587 



ites, such as occurs in many acute diseases, especially in pneumonia and 
typhoid fever, it has been found advantageous to add various drugs to 
the cleansing enema. An effective combination contains one dram of 
turpentine, two of ox-gall, three of milk of asafetida to eight ounces 
of soap-suds. 

Any of these cleansing enemata may be reinforced by the addition 
of half an ounce or an ounce of glycerine, which not only aids in soften- 
ing the fecal material, but by its hygroscopic effect intensifies the action 
of the injection. 

A distinction is commonly made between a low and a high enema. 
An injection syringe with a simple hard-rubber nozzle is often employed 
for the introduction of the fluid, which under these conditions hardly 
passes beyond the rectum. It has been found more advantageous to have 
the fluid, as a rule, pass as far into the colon as possible. To accomplish 
this the patient must be recumbent with the hips elevated, while a soft- 
rubber rectal tube or large-sized catheter attached to douche-pipe is 
passed as far as possible into the rectum. There is doubt whether the 
tube, no matter how long, passes beyond the rectum, but the fact remains 
that by these means the fluid is carried higher than under the older pro- 
cedure, and the colon is more thoroughly emptied. Such an enema is 
commonly termed a "high enema." 

2. Nutrient. — Various forms of nutritive enemata are employed. The 
• basis of all is milk, from 6 to 8 ounces, to which are usually added one 

or two eggs and a teaspoonful of common salt. This mixture should be 
thoroughly peptonized. Some add from one-half to one ounce of lactose 
or glucose to the mixture. If stimulation is desired, whiskey or other 
medicine can be given at the same time. Since opium has no local effect, 
the custom of adding this drug to an enema in the hope of allaying irri- 
tability of the rectum is not well founded. A hypodermic of morphine 
would be much more effective. 

One hour before giving a nutritive enema, the rectum and colon 
should be thoroughly emptied by a high enema, and after it the patient 
should be kept perfectly quiet for at least an hour. 

For the introduction of a nutritive enema a simple funnel attached by 
not more than a foot of rubber tubing to a rectal tube or large catheter 
should be used, and no more force employed in its introduction than is 
necessary. The funnel should be raised just sufficiently to allow the 
fluid to pass into the bowel. The retention of nutritive enemata depends 
largely upon the gentleness with which they are administered. The 
tube must be withdrawn most carefully. 

3. Therapeutic. — Many drugs can be given by rectum. The dose is 
commonly twice that given by mouth. Bromides, chloral, paraldehyde, 
and other disagreeable sedatives may be given in this manner. Stimu- 
lants such as whiskey and coffee, simple saline solution, digitalis and 
the like may be likewise administered. In giving such enemata the 
irritating qualities of the substance to be given must be borne in mind. 



588 



APPENDIX 



and dilution with water or normal salt solution practiced accordingly. 
The total quantity should not, however, exceed six or eight ounces. 

Colon Irrigation. Lavage of the Colon. — In dysentery, typhoid 
fever, colitis of various forms, and also in various types of intoxication', 
anemia, chronic rheumatism, and the like, the irrigation of the colon 
with large quantities of warm normal salt solution may be employed. 
The solution at a temperature of about 110° F. is held in a large douche- 
bag or other reservoir. A double rectal tube (Kemp's) with one chan- 
nel for the entrance and another for the outflow of the fluid is commonly 
employed. With this apparatus from one to two gallons of warm salt 
solution is allowed to flow slowly in and out of the bowel in the course 
of from 30 minutes to an hour. The patient lies ordinarily upon the 
back or the left side. The knee-chest position is recommended if it is 
desired to carry the fluid as high as possible in the colon, but it is too 
trying for general use. 

Instead of the double tube a single rectal tube with a "T" attach- 
ment may be employed, the solution being run in through one arm of 
the "T" till the bowel is moderately distended and then allowed to 
escape through the other arm, which is made to empty into a receiving 
vessel. 

Enteroclysis. — The more slowly the solution flows in and out the 
more of it will be absorbed. Murphy, of Chicago, has recently sug- 
gested the advantage of allowing salt solution to drip into the bowel 
continuously for hours with the object of its slow but steady absorption. 
If it is desired to hasten the process the reservoir is suspended just 
sufficiently above the level of the patient's body to cause the fluid to 
flow very slowly into the rectum. In this way about a pint of normal 
salt solution may be given and absorbed in an hour. 

Hypodermoclysis. — Normal salt solution to the amount of 500 c.c. 
to 1,000 c.c. may be injected into the soft cellular tissues of the skin, 
and thence be gradually absorbed into the circulation. An ordinary 
douche-bag armed with an aspirating needle may serve the purpose, but 
in most hospitals more satisfactory apparatus is in use. The salt solution 
is sterilized in flasks holding 1,000 c.c. The flask is placed at the head 
of the bed about 3 feet above the level of the patient's body. From 
the flask rubber tubing, weighted at the end to keep it in the flask, 
leads to the clysis needles. Near the end a glass "Y" is inserted to 
either arm of which one of the needles is attached. The ordinary aspir- 
ating needles may be used, but the finer the needle the slower will be 
the flow of the solution and the less traiunatism will be done. In emer- 
gencies it may be desirable to introduce the fluid as rapidly as may be. 
In most cases, however, it is best to make the injection as slowly as 
possible, an hour or two being occupied in the administration of 1.000 
c.c. If fine needles are used, the patients may be quite undisturbed by 
the procedure, and the injections may be frequently repeated. The usual 
sites chosen are the pectoral or lateral thoracic regions, but the injec- 



GENERAL CARE OF THE SICK 



589 



tions may be made into any of the loose cellular tissue. Perfect asepsis 
must be practiced as to the fluid, apparatus and the hands of the opera- 
tor. Care should also be taken to exclude air from the tubing before 
beginning the injection. The sites of puncture are to be protected by 
pads of sterile gauze. 

Intravenous Infusion of Normal Salt Solution. — The solution 
may be introduced directly into a vein, usually the median basilic or 
median cephalic vein. For this purpose a ligature is bound about the 
arm to make the veins stand out. Usually the selected vein is then ex- 
posed and two ligatures passed under it close to one another and left 
untied. The vein is then nicked between the ligatures on one side and 
into the opening a special small canula connected by tubing to the flask 
of salt solution as for hypodermoclysis is introduced. One of the ligatures 
then secures the canula in the vein, while the other ties off the vein 
below. As soon as the canula is safely in the vein the ligature on the 
arm is cut, and the solution is allowed to flow slowly into the vein. 
Here again it is desirable to make the injection slowly, that the heart 
may not be embarrassed by too sudden an increase of its contents. 

A much simpler method will ordinarily answer the purpose. The 
arm is ligatured as before, and when the veins are well distended a small 
aspirating needle is thrust obliquely into one of them. As soon as a 
free flow of blood from the needle indicates that it is in the vein, the 
rubber tubing leading from the flask is slipped over the end of it and 
the fluid is allowed to flow as before. It is, of course, necessary to start 
the flow of the solution through the tubing before connecting it to the 
needle. After the procedure the seat of puncture should be protected 
by a pad of sterile gauze. 

Bleeding. — The withdrawal of blood from the arm is usually effected 
in the ancient manner of constricting the upper arm and then opening 
the median basilic or median cephalic veins at the elbow. From 8 to 16 
ounces of blood are withdrawn. 

Blood may be drawn from one of these veins by an aspirating appa- 
ratus. To prevent the clotting of the blood in the tubes or needle sterile 
liquid albolene is first drawni through them. .The aspirating needle is 
plunged obliquely into the distended vein exactly as for an intravenous 
injection. Perfect asepsis must be observed in either procedure. 

Baths. — Cold Sponge. — Water at ordinary temperature, 65° to 
70° F., may be used or the temperature may be raised or lowered as 
desired, the colder the water, naturally the more effective it will be in 
reducing temperature. The patient's loins are covered by pinning a 
towel around him. The bed is protected by rubber sheeting. The patient 
is then uncovered and sponged from head .to feet, front and back. The 
sponging should alternate with gentle friction of the skin by the nurse's 
hand. For this reason it is well to have two nurses. Such a bath is 
usually given for 15 or 20 minutes. 

Alcohol Sponge. — Alcohol in varying proportions is added to the 



590 



APPENDIX 



water for this purpose. From 25 to 50 per cent, is commonly used. 
The more rapid evaporation of the alcohol intensifies the effect of the 
bath, and its addition is usually grateful to the patient. Whenever such 
a bath is given care should be taken to wet the head, or a cold wet cloth 
should be kept upon the forehead. 

Tub Baths. — Cold. — The Brandt method is described on page 330. 

Hot. — For a hot bath it is best to fill the tub with water at a tem- 
perature of 90° to 95° F., and after the patient is immersed further raise 
the temperature by adding more hot water. In this way the tempera- 
ture may be raised to 105° to 110° F. The head should be constantly 
wet with cool water. Such a bath may be continued for 15 or 20 minutes. 
On leaving it the patient may be sv/athed in blankets and the perspira- 
tion induced by the bath thus protracted for half an hour. When only 
a sedative effect is sought from such a bath, the temperature should not 
exceed 100° F. 

Hot-air Bath. — The bed is protected by rubber sheeting, covered by 
a blanket on which the patient lies. The body of the patient is covered 
by bed-cradles supporting several layers of blankets, which are tucked 
closely about the neck and under the patient's feet. The hot-air 
apparatus ordinarily consists of a length of small-sized stove-pipe, large 
enough at one end to hold an alcohol lamp and tapering toward the 
other end, which is also bent at an angle so as to render it easy to intro- 
duce it under the bed-clothing at the foot of the bed. The portion of 
the pipe likely to be touched by the blankets must be protected by 
asbestos or wet cloths. When the bed has been arranged to make the 
air-chamber about the patient's body as tight as possible, the alcohol 
lamp is lighted and placed in the lower end of the pipe through a trap- 
door provided for the purpose, and the door closed. The air above the 
patient should reach a temperature of 150° to 175° F. The head must 
be kept cool by an ice-cap or cold wet cloth. Unless fluids are restricted, 
water, hot tea or lemonade may be given during the bath, which should . 
be continued for 20 minutes or more after the desired temperature has 
been reached. The bath over, the patient should be rubbed dry, rolled 
in dry blankets, and allowed to lie quiet for an hour, with the ice-cap 
to his head and a hot-water bottle at the feet. 

At the end of this time the body is rubbed with alcohol and the . 
bath is over. 

Cabinet-haths. — Portable cabinets arranged to fit closely about the 
neck of a patient and surround the body as he sits in a chair, are com- 
monly employed. The heat is supplied by an alcohol lamp or gas- 
burner placed under the chair. 

Electric-light cabinets in which the heat is supplied by numbers of 
incandescent lights are also employed for this purpose. They are safe 
and very easily managed. 

The Hot Pack. — Dry. — The patient is wrapped in several layers 
of blankets with hot-water bottles at the feet, between the legs and in 



GENERAL CARE OF THE SICK 



591 



each axilla. Instead of the hot-water bags bricks heated in an oven 
may be used. Care must be taken to wrap bags or bricks in such a way 
as to prevent burning the patient. The head is cooled as in the hot- 
air bath and hot drinks may be given. The pack is continued for half 
an hour, and then terminated like a hot-air bath. 

Wet. — For the wet hot pack blankets wrung out of water heated to 
150° F. are used. The patient is swathed in these, and hot-water bottles 
placed as for the dry pack. The head must likewise be kept cool, and 
the hot drinks may be given. The pack should be continued about one- 
half an hour, and then terminated like a hot-air bath. 

Cold Pack. — With the bed protected, the patient is wrapped in a 
sheet wet in cold water of any desired temperature, and the sheet is 
frequently sprinkled with more water during the course of half an 
hour in which the patient remains in the pack. Throughout the process 
vigorous rubbing is kept up through the sheet. When the pack is ended 
the body should be rubbed thoroughly dry. 

Local Hot or Cold Applications. — Priessnitz compress. The 
chest, abdomen or any of the extremities may be treated by compresses 
wrung out of water either hot or cold, as may be desired. The com- 
presses must be frequently changed to maintain as nearly as possible 
the temperature desired. 

Mustard Paste. — Mustard and flour are mixed usually in the pro- 
portion of 1 to 4 or 6 for an adult, and then stirred into a paste with 
a little cold water. The paste is spread on gauze or cheesecloth of any 
desired size, and applied to the surface of the body. The other sur- 
face should be covered by more gauze or linen. Mixing the white of 
an egg or a little oil with the paste is said to lessen the risk of blister- 
ing. The action of the paste on the skin must be frequently observed, 
and the .application removed when the skin is well reddened. The 
area treated should then be washed with warm soap and water to 
remove any of the application still adhering to the skin, and, if very 
red, anointed with vaseline. 

Flaxseed Poultice. — To about a pint of boiling water enough flax- 
seed meal is slowly stirred in to make a paste just thin enough to drop 
from a spatula or spoon. Thorough beating of the mixture is said 
to make it "lighter." The hot meal is then spread on gauze or cheese- 
cloth, the reverse side covered by more gauze and applied to the de- 
sired surface of the body. A further covering of oiled silk serves to 
retain the heat. Such a poultice will keep hot for about an hour, and 
should then be removed. The reddened area is covered by cotton. 

As a matter of convenience the paste known as cataplasma kaolini 
may be used instead of the flaxseed. 

Ice Coil. — The coil consists of small-sized rubber tubing (7 mm. 
in diameter) fastened in a coil about 25 cm. diameter. One end of the 
coil is led up to a tub. of ice-water several feet above the level of the 
patient's body, the other end empties in a receiving pail. The water 



592 



APPENDIX 



is started through the coil by suction. The coil is commonly applied 
to the abdomen, but may be used on the head. When working per- 
fectly it is very effective in reducing the local temperature, but it must 
be constantly watched to be sure that the flow has not been stopped 
by some accidental kinking of the tubing. 

STANDARD DIETS 

The amount of food necessary varies greatly under different condi- 
tions of health, and still more markedly in disease. Age and weight, 
bodily activity and climate have important influence upon it. It un- 
doubtedly varies in different individuals under apparently like condi- 
tions. For a man at rest it is calculated that the daily ration should 
contain approximately 35 calories per kilogram of body weight. For a 
child one year old the ratio is 90 calories per kilo ; at two years, 80 ; at 
ten years, 60, and at fourteen years, 52. On this basis it is estimated an 
adult of about 150 pounds w^eight (70 kilograms), resting, wwld require 
a daily ration representing about 2,500 calories. 

The distribution of these values between the several food princi- 
ples is a subject much studied and discussed. Voit's standard allowed 
100 to 120 grams of protein per day. Chittenden flnds that healthy men 
may require only 40 to 60 grams of protein. Other calculations exceed 
Voit's standard. As an average one may say that the 2,500 calories 
may be drawn from 100 grams of protein, 50 grains of fat, and 400 
grams of carbohydrates. 

In febrile conditions, especially in typhoid fever, there is a rapid 
loss of weight, ascribed to destruction of the protein of the body as a 
result of toxemia. To meet this loss it is calculated that the typhoid- 
fever patient requires 40 calories per kilo., or for the patient of 70 kilo- 
grams 2,800 to 3,000 calories. Efforts to bring the typhoid dietary up 
to this standard by feeding cream, lactose and other carbohydrates 
freely have apparently been advantageous. How generally this exam- 
ple may be followed or with what advantage is not yet known. 

In most hospitals we flnd in use a series of diets which under ordi- 
nary conditions are employed in the treatment of the sick. These, for 
convenience, are designated as fluid diet, soft diet, convalescent diet. 

Fluid Diet. — ]\Iilk, beef tea, chicken broth, mutton broth, egg 
albumin ; 6 to 8 ounces of one or the other every 2 or 3 hours. 

Soft Diet. — Gruels, junket, custard, cereals, eggs (boiled or 
poached), milk toast, farinaceous puddings, tea, coffee, milk. These 
feedings may be given every 2 or 3 hours still, or grouped in three 
meals with lighter feedings between. 

Convalescent Diet. — This is regularly arranged in three meals, as 
follows : 

Breakfast. — Tea or coffee with milk or cream and sugar. Bread 
and butter — white bread or graham bread, or cornbread, or rolls, or 



STANDARD DIETS 



593 



toast. Porridge: hominy, farina or other cereal. Meats: eggs, fish, 
bacon. 

Dinner. — Soup — stock, or chicken, or mutton broth with barley or 
vegetable. Bread and butter. Meats — beef, roast or broiled. Chicken 
or fish. Vegetables — potatoes, mashed or baked, rice, macaroni, hom- 
iny, peas, beans (string), spinach, etc. Puddings, rice, bread, farina, 
tapioca, corn starch or custard. 

Supper. — Tea with cream or milk, and sugar. Bread and milk, 
milk toast, bread and butter, toast and butter. Cooked fruits, such as 
apples, stewed or baked, or as apple sauce, stewed prunes or pears. 

To the supper any of the articles enumerated under soft diet are 
added when ncjcessary. 

Low Salt or Salt-free Diet. — The quantity of salt in any of these 
diets may be reduced to a minimum by withholding salt in the prepara- 
tion of the food and allowing no salt with the meals. In each instance 
a small quantity of sodium chloride naturally present in the several 
foods remains. For the majority of cases the salt diet thus modified is 
employed when such a reduction of the salt intake is desired. 

Under most conditions the fluid, soft and convalescent diets are or- 
dered in succession with no thought to the quantitj^ of food taken or the 
value of the diet as a whole. The acutely sick patient is ordered a fluid 
diet, and with the return of appetite, which usually accompanies the 
subsidence of fever or pain, the soft diet is given, and later the conva- 
lescent. In cases of protracted illness it may be of great importance to 
be able to calculate the amount and the value of the food taken and to 
determine its sufficiency. 

Under the supervision of Dr. H. S. Carter the effort has been made 
to learn the appropriate composition and food value of the food actually 
received by the patients. For this purpose a sample diet of each class, 
that is, the equivalent of a diet actually served in the wards in the course 
of the regular work, was taken, the amounts of the several foods deter- 
mined, the whole mixed together, dried in bulk, reduced to a powder, 
and then analyzed for the chief constituents with the following results : 

FLUID DIET 

Quantities Given 

gms. 



Coffee 164 

Broth 676 

Griiol (Oatmeal) 202 

Tea 200 

Milk 600 

Sugar 67 

Lemon juice 35 

Egg albumin 92 



2036 

This diet is served in quantities of about 6 ounces (180 gms.) every two hours. As 
the patients are allowed considerable choice the amounts of the several foods will vary 
in different cases. The sugar and part of the milk are given with the coffee and tea, 
the lemon juice with the egg albumin. 
38 



594 



APPENDIX 



Gms. 

Toast 12 

Bread 41 

Sugar 19 

Oatmeal 83 

Milk 215 

Coffee 170 

Butter 6 

Egg (no shell) 45 

591 



SOFT DIET 

Quantities Given 
Dinner 

Gms. 

Broth 165 

Bread 12 

Potato with skin. 95 

Rice boiled 107 

Corn starch 80 

Ice cream 42 

501 



Supper 

Gms. 

Bread 30 

Toast 30 

Farina 91 

Butter 8 

Apple sauce 133 

Sugar 12 

Tea 180 

Milk 210 

704 



Breakfast 



Lean meat. 



Gms. 

. 33 



CONVALESCENT DIET 

Quantities Given 
Dinner 



Lamb. 



Gms. 



Corn Bread 45 String beans 37 



Toast 20 

Sugar 26 

Oatmeal (cooked) 55 

Butter 5 



Boiled rice 80 

Cup custard . . . . « 124 



Supper 

Gms. 

Milk 170 

Tea 180 

Bread 29 

Cup custard (sweetened) 71 



Bread 18 Farina 85 

Vegetable soup. ....... 200 Cooked prunes (little 



Milk. 200 Tapioca pudding (sweet- 
ened) 63 



Coffee 200 



Potato with skin 
(baked) 20 gms 163 



sweetened) 
Sugar . 



33 



Butter 17 



594 773 683 

SALT-FREE DIET (SOFT) 

Quantities Given 

Breakfast Dinner Supper 

Gms. Gms. Gms. 

Bread 28 Sugar. 11 Egg (1) 29 

Sugar 11 Bread 28 Toast 14 

Farina 55 Butter 19 Bread 22 

Butter. 26 Rice 69 Butter 15 

Egg (1) 29 Farina 106 Custard (sugar 15) ... . 102 

Coffee 150 Tea 160 Prunes (sugar 15) 63 

Tea 190 



299 



393 



435 



ANALYSES OF DIETS 





Fluid Diet 


Soft Diet 


Convalescent 
Diet 


Salt Free 
Soft Diet 




Gms. 


Gms. 


Gms. 


Gms. 


Total weight 


2045.5 


1756. 


2054.50 


1593. 




1830. 


1393.5 


1594.50 


1317. 


Protein (estimated) 


47.32 


49.48 


89.35 


34.53 




7.57 


7.91 


14.29 


5.52 


Fat 


28.01 


49.95 


70.09 


65.16 


Carbohydrate 


108.98 


291.24 


256.02 


140.76 




898.59 


1878.88 


2128.42 


1257.70 


Chlorides 


2.67 


3.36 


5.31 


.96 



STANDARD DIETS 



595 



Caloric Value of a Diet. — To obtain this accurately we must make 
such analyses as those above or know the exact amounts of each food 
consumed and the chemical composition of each. Each gram of fat is 
equivalent to 9.3 calories, and each gram of protein or carbohydrate to 
4.1 calories. In ordinary practice it is difficult to carry out these pro- 
cedures, but the value of the diet can be obtained with sufficient accu- 
racy by the aid of such a table as the following: 

TABLE OF FOOD-VALUES IN UNITS OF 100 CALORIES 



Milk, 5 oz 5. 

Cream, 16 per cent. (2 oz. ) 1,5 

Beef tea, 21/2 pints 10.0 

Gruels, without milk, 10 oz 4.0 

Buttermilk, one and one-half glasses (9.5 oz.) 8. 

Koumis, one glass (7 oz.) 5. 

Whey, two glasses (13 oz. ) 3.5 

Eggs, one and one-half 10. 

Egg albumin (whites of 2 eggs to G ounces water), 3 glasses 24. 

Whites of eggs, 6 24. 

Yolks of eggs, 2 4.5 

Custards, 4 oz 7.0 

Oatmeal, one and one-half serving (5.5 oz.) 4.25 

Boiled rice, ordinary cereal dish (3 oz. ) 2.5 

Hominy, large serving (4.2 oz. ) 2.5 

White bread, home made, one thick slice (1.25 oz. ) 3.2 

One small Vienna roll (1.25 oz.) 3.2 

Butter, one pat (1.5 oz.) 0.0 

Sugar, three teaspoonfuls, one and one-half lumps (0.8 oz.) 0.0 

Oil, one-third ounce O.Q 

Codfish, two servings (5 oz.) 23. 

Halibut steaks, one serving (2.8 oz. ) 15. 

Mackerel, Spanish, one serving (2 oz. ) 12.2 

Shad, one serving (2.1 oz. ) 11.2 

Salmon, small serving (1.5 oz.) 7.3 

Oysters, 12 12. 

Roast beef, ordinary serving (1.8 oz.) 10. 

Small sirloin steak (1.4 oz. ) 7.5 

Leg of lamb or mutton, ordinary serving (1.8 oz.) 10. 

Lamb chop, one small (1 oz. ) 6. 

Bacon, small serving, medium fat (0.5 oz.) 1.5 

Chicken, broiler, edible portion, large serving (3.2 oz.) 10. 

Turkey, large serving (1.2 oz.) 7. 

Potato, baked, one, good size (3 oz. ) 3.75 

Potato, sweet, baked, one-half average potato (1.7 oz.) 1.5 

String beans, five servings ( lO.Of) oz.) 3.75 

Spinach, two ordinary servings (0.1 oz.) 3.7 

Peas, green, one serving (3 oz.) 5.7 

American or Swiss cheese, 1.5 cubic inches (0.75 oz. ) 0. 

One baked apple, 3.3 ounces 0.5 



596 



APPENDIX 



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INDEX 



Abasia, 577 

Abducens nerve, 488 

Aboulia, 56" 

Abscess, appendicular, 98 

of brain, 539 

of liver, 125 

of lung, 37 

following pneumonia, 24 
hemoptysis in, 14 
metastatic, 38 

of pancreas, 138 

of spleen, 264 

perinephritic, 173 

retropharyngeal, 60 

subphrenic, 145 
Achondroplasia, 293 
Acliylia gastrica, 82 
Acromegaly, 580 
Actinomyces, 427 
Actinomycosis, 426 
Addison's disease, 262 
Adenitis, in diphtheria, 358, 3G0 

in scarlet fever, 349, 350 

in glandular fever, 419 

tubercular, 409 
Adenoids, 62 

Adrenals, diseases of, 262 
Agraphia, 548 
Ague cake, 438 
Akoria, 82 

Albuminuria, febrile, 154 
hemic, 154 
nervous, 154 
physiological, 153 

without definite kidney lesions, 153 

with definite kidney lesions, 154 
Alcohol and endocarditis, 188 

in pneumonia, 27 
Alcoholism, acute, 296 

chronic, 297 
Allorrhythmia, 220 
Amaurosis, 487 
Amaurotic family idiocy, 549 
Amblyopia, 545 
Ameba dysenteria?, 95 
Amyloid degeneration, of kidnev, 168 

of liver, 129 

of spleen, 264 
Amyotrophic lateral sclerosis, 510 
Anacidity, 82 
Analgesia, 520 
Anaphylaxis, 12 
Anemia, 246 

pernicious, 247 
blood in, 249 

primary, 246 

secondary, 247 

splenic, 264 



Anesthesia, 519, 520, 566 

dissociative, 519 
Aneurism, 232 

definition, 232 

diagnosis, 237 

etiology, 233 

morbid anatomy, 233 

of ascending arch, 234 

of descending arch, 236 

of thoracic aorta, 236 

of transverse arch, 235 

physical signs, 234 

prognosis, 237 

treatment, 237 
Angina pectoris, etiology, 226 

morbid anatomy, 226 . 

symptoms, 226 

treatment, 227 
Angina, toxic, 227 
Angiocliolitis, acute catarrhal, 131 

chronic catarrhal, 131 

suppurative, 132 

ulcerative, 132 
Animal parasites, 429 
Ankylostomum duodenale, 469 
Anopheles, 430 
Anosmia, 485 
Anthracosis, 33 
Anthrax, 425 

external, 425 

internal, 426 

intestinal, 426 
pulmonary, 426 
Antidiphtheritic serum, 362 
Antimeningitic serum, 531 
Antitetanic serum, 417 
Antitoxin in diphtheria, 363 

in tetanus, 417 
Anuria, 152 

Aoitic insufficiency, 195 

stenosis, 198 
Aortitis, acute, 229 

chronic, 229 
Aphasia, 535, 547 

intercortical, 548 

motor, 548 

sensory, 547 
Aphemia, 548 
Apoplexy, cerebral, 533 
Appendicitis, acute, 96 

abscess in, 98 

bacteriology, 97 

blood, 99 

diagnosis, 101 

etiology, 96 

morbid anatomy, 97 

prognosis, 101 

svmptoms, J)7 

treatment, 101 

597 



598 



INDEX 



Appendicitis, chronic, 98, 100 
Aran-Duclienne type of lead palsy, 302 
Argyll-Robertson 'pupil, 489, 512,^542 
Arrhvtlimia, cardiac, 201, 221 

classification of, 224 
Arsenic poisoning, 303 
Arsenobenzol, 450 
Atrophy, Aran-Duchenne type, 510 

Ijrown, 231 

Duchenne type, 510 

in syringomyelia, 519 

of optic nerve, 487, 512 

of stomach, 67 

progressive muscular, 509 
Arteriosclerosis, 229 

and endocarditis, 188, 192 

and nephritis, 165 

course, 232 

etiology, 229 

morbid anatomy, 230 

symptoms, 231 

treatment, 232 
Arteritis, chronic, 229 
Arthritis, acute, following pneumonia, 25 

gonorrheal, 383 

in scarlet fever, 350 

in typhoid fever, 326 

rheumatic, 379 
Arthritis deformans, see Polyarthritis, 
275 

Ascariasis, 464 

Ascaris lumbricoides, 464 

Ascites, 147 

in cancer of the liver, 127 

in cirrhosis of the liver, 121 

in heart disease, 192 

in nephritis, 161, 164 

in Banti's disease, 265 
Aspergilli, 428 
Aspiration, of chest, 48 
Aspiration pneumonia, 28 
Astasia-abasia, 577 
Asthma, bronchial, 12 

cardiac, 192 

renal, 157 

thymic, 5 

with hay fever, 12 
Ataxia, hereditary cerebellar, 517 
Friedreich's, 517 
locomotor, 512 

course and prognosis, 514 
diagnosis, 514 
etiology, 512 
morbid anatomy, 512 
symptoms, 512 
treatment, 515 
Atelectasis. 17 
Auditory nerve. 491 
Aura, 7)55 

Autumnal catarrh, 2 

Babinski reflex, 504, 526 
Ba coin's sign. 51 

Bacillus ai'rogenes ca])sulatus, 142 



Bacillus diphtherise, 58, 185, 305, 356 
dysenterise, 94 
enteridis, 305 
Friedliinder's, 19 
influenzae, 19, 337 
leprae, 4] 5 
mallei, 422 
pestis, 343 
Pfeiffer's, 337 
proteus, 143 
pyocyaneus, 143 
typhoid, 19, 185, 313 
tj'phoid or colon, 19, 133, 143, 185, 
305 

Bacteremia, 374 
Bacterial poisons, 305 
Balantidium coli, 462 
Banting, 295 
Banti's disease, 264 
Basedow's disease, 268 
Baths, alcohol sponge, 589 

Brandt, 330 

cabinet, 590 

cold sponge, 589 

hot, 590 

hot air, 590 
Bell's mania, 549 
Bends, the, 503 
Beri-beri, 345 
Biedert, ganglia of, 218 
Bile-ducts, diseases of, 131 
Bilharzia hematobia, 464 
Biliary colic, 135 
Black' death. 342 
Black fever, 420 
Black sickness, 461 
Black-water fever, 440 
Blastomvcetes, 428 
Bleeding, 589 

Blood, in acute meningitis, 529 
in chlorosis, 246 
in chronic tuberculosis. 400 
in gout, 280 
in hemophilia, 258 
in Hodgkin's disease. 254 
in lead poisoning, 302 
in malarial fever, 436, 437 
in pernicious anemia, 249 
in pseudoleukemia, 254 
in purpura. 256 
in relapsing fever. 335 
in secondary anemia. 247 
in sypliilis. 447 
in typhoid fever. 324 
in typluis fever. 334 
in uncinariasis. 470 
Blood cultures, in anthrax. 426 

in leprosy, 414 

in ]\[alta fever, 345 

in i)lagne. 344 

in ])neumonia. 25 

in sei)ticemia. 375 

in sejitic endocarditis, 186 

in ty])hoid fevei', 327 



INDEX 



599 



Blood poisoning, 374 
Blood pressure, 207 
Blue babies, 229 
Blue disease, 420 
Blue line, 302 
Boas-Oppler bacillus, 75 
Bothriocephalus latus, 476 
Bowels, diseases of, 83 
Brachial plexus, 497 
Bradycardia, 201, 216 
Brain, abscess of, 539 

anemia of, 531 

cysts of, 544 

diseases of, 523 

edema of, 532 

fever, 549 

hemorrhage into, 532 

hyperemia of, 531 

sclerosis of, 543 

tumors of, 544 
Brandt bath, 329 
Break-bone fever, 339 
Breast, pigeon, 63 
Bright's disease, see Nephritis, 160 
Bronchial asthma, 12 
Bronchiectasis, hemoptysis in, 14 

with chronic bronchitis, 9 

with emphysema, 35 
Bronchiolitis exudativa, 12 
Bronchitis, acute, 7 

in anthrax, 425 

in bronchopneumonia, 28 

in coryza, 1 

in influenza, 337 

in measles, 353 

in tuberculosis, 390, 394, 397 

in typhoid fever, 319-326 

in whooping-cough, 369 
Bronchitis, capillary, 28 
Bronchitis, chronic, 9 

with bronchiectasis, 11 

with emphysema, 36 

with fibroid phthisis, 405 

with gout, 281 

with heart disease, 192 

with interstitial pneumonia, 32 

with pneumoconiosis, 33 
Bronchitis, fibrinous, 10 
Bronchopneumonia, aspiration, 28 

deglutition, 28 

diagnosis, 30 

etiology, 28 

morbid anatomy, 29 

physical signs, 30 

prognosis, 31 

symptoms, 29 

treatment. 31 
Brudzinski's signs, 527 
Bubonic plague. 342 
Bulbar paralysis, asthenic, 311 

progressive, 511 
Bulimia, 82 

Cachexia, malarial, 438 



Caisson disease, 502 
Calculi, biliary, 134 

nephritic, 171 

pancreatic, 141 

renal, 171 
Cancer, of brain, 544 

of cord, 522 

of esophagus, 65 

of intestine, 102, 113 

of kidney, 174 

of liver, 127 

of lung, 41 

of pancreas, 140 

of pericardium, 182 

of peritoneum, 147 

of spleen, 204 

of stomach, 73 

of thymus, 274 

of thyroid, 268 
Gancrum oris, 58 
Carbonic monoxide poisoning, 307 
Carcinoma, see Cancer 
Carditis, 212 
Care of eyes, 585 

of feet, 586 

of hands, 586 

of mouth, 586 

of skin, 585 
Catarrh, autumnal, 2 

acute gastric, 65 

chronic, 67 

of bile-ducts, 131 

of intestines, 83 
Cercomonas intestinalis, 462 
Cerebellum, tumors of, 546 
Cerebrospinal fever, 524 
Cestoda, 462, 475 
Clialicosis, 33 
Charcot joints, 514 
Charcot-Leyden crystals, 13 
Cheyne-Stokes respiration, 534 
Chicken-pox, 458 

Chlorides of urine, in lobar pneumonia, 22 

in nephritis, 159 
Chlorosis. 246 

blood in, 246 

diagnosis, 247 

etiology, 246 

symptoms, 246 

treatment, 247 
Choked-disk, 487-545 
Cholangitis, acute catarrhal, 131 

chronic catarrhal, 131 

suppurative. 132 
Chol('f\siitis. aciiic infectious, 132 
Cholelithiasis, diagnosis, 136 

etiology, 133 

morbid anatomy, 134 

prognosis, 137 

symi)toms, 134 

tnvitmoit, 137 
Cholemia, 123 
Cholera asiatica, 90 

complications, 92 



600 



INDEX 



Cholera, diagnosis, 92 

etiology, 90 

morbid anatomy, 91 

prognosis, 92 

symptoms, 91 

treatment, 92 
Cholera infantum, 87 
Cholera morbus, 85 
Cholera nostras, 85 
Chorea, acute, 551 

in endocarditis, 1S7 

in rheumatic fever, 3S2 

minor, 551 

Sydenham's, 551 
Chvostek's sign, 563 
Chylopericardium, 182 
Chyluria, 154, 472 
Circulatory system, diseases of, 175 
Circumflex nerve, 497 
Cirrhosis, atrophic, 120 

course, 123 

diagnosis, 123 

etiology, 120 

morbid anatomy, 120 

prognosis, 123 

symptoms, 121 

treatment, 123 
Cirrhosis, biliary or Hanot's, 124 

course, 124 

diagnosis, 124 

etiology, 124 

morbid anatomy, 124 

symptoms, 124 

treatment, 124 
Cirrhosis, of liver, 120 

alcoholic or atrophic. 120 

fatty, 121 

Hanot's or biliary. 124 

Laennec's or portal, 120 
Cirrhosis ventriculi, 67 
Clavus hystericus, 566 
Clubbed fingers, 11 
Coagulation time, 256 
Cocaine habit, 301 
Cocaine looisoning, 301 
Cocainism, 301 
Coin-test, 55 
Colic, biliary, 135 

lead. 301 

mucous, 112 

renal, 171 
Colitis, see Enteritis, 83 
Colitis, croupous, following pneumonia, 25 

mucous, 112 

ulcerative, 90 
Collapse of lung, 17 
Colles' law, 442 
Colon, irrigation of, 588 

lavage of. 588 
Coma, alcoholic, 296 

apoplectic, 534 

diabetic, 286 

epileptic, 556 



I Coma, uremic, 157 
Comma bacillus, 90 
Compensation, 190 
failure of, 190 
causes of, 191 
Compressed-air disease, 502 
Compression myelitis, 505 
of cord, 505 
of lung, 17 
Condylomata, 443 
Congestion of lungs, active, 15 
and hemoptysis, 14 
hypostatic, 15 
in heart disease, 192 
in lobar pneumonia, 19 
Congestion, in heart disease, 191 
Constipation, 107 
etiology, 107 

in chronic congestion, 192 

symptoms, 108 

treatment, 108 
Constitutional diseases, 275 
Consumption, see Tuberculosis 

galloping, 394 

pulmonary, 396 
Convulsions, of children, 553 
infantile, 553 

in brain tumor, 545 

in epilepsy, 556 

in hysteria, 567 
Cor bovinum, 196 
Cord, spinal, anemia of, 501 
diseases of, 499 
embolism of, 501 
hemorrhage into, 502 
hyperemia of, 501 
thrombosis of, 501 
tumors of, 522 
Coronary arteries, disease of. 213. 214 
Coryza, acute, 1 
Cranial nerves, diseases of, 485 
Craniotabes, 291 
Cretinism, 272 
Crises, Dietl's, 151 

visceral, 512 
Crisis of pneumonia, 20 

pseudo, 20 
Croup, membranous, 359 

spasmodic, 5 
Crus, tumor of, 546 
Curschmann's spirals. 13 
C3"anosis. in congenital heart disease, 228 

in emphysema. 36 

in heart disease, 192 

in pericarditis, 177 

in pneumonia, 21, 29 
Cysticercus cellulosa^, 479 
Cvstinuria. 155 
Cysts, hydatid. 479 

ovarian. 148 

pajicreatic. 140 

renal. 169 
Cytology of pleural fluids, 48 
Cytorrhyctes variohr, 452 



INDEX 



601 



Deafness, from meningitis, 528 
from scarlet fever, 350 
in leukemia, 251 
word, 535, 547 
Death, sudden, in angina, 227 

in aortic insufficiency, 198 
in disease of coronary arteries, 
214 

in myocarditis, 214 

in status lymphaticus, 262 

in thymus enlargement, 274 

Deglutition pneumonia, 28 

Delirium, acute, 549 
tremens, 298 

Dementia paralytica, 540 

Dengue, 339 

Dermacentor occidental is, 420 
Dermatomyositis, 309 
Desquamation of measles, 358 

of rubella, 355 

of scarlet fever, 354 
Diabetes insipidus, 289 

diagnosis, 290 

etiology, 289 

morbid anatomy, 289 

symptoms, 290 

treatment, 290 
Diabetes mellitus, 284 

acetone in, 287 

coma in, 286 

course and prognosis in, 287 

diacetic acid in, 287 

diagnosis of, 287 

etiology of, 284 

gangrene in, 286 

metabolism in, 285 

morbid anatomy of, 285 

oxybutyric acid in, 288 

symptoms of, 286 

treatment of, 287 

urine in, 286 
Diarrhea, fermentative, 87 

in appendicitis, 98 

in childhood, 86 

in chronic congestion, 192 

in enteritis, 83 

inflammatory, 87 

in tuberculosis, 400 

in uremia, 157 

mucous, 112 

summer, 86 
Diathesis, lithemic, 281 

urid acid, 281 
Diazo reaction, 327 
Dibothriocephalus latus, 476 
Dietl's crises, 151 
Diets, analyses of, 594 

caloric value of, 594 

convalescent, 592 

fluid, 592 

salt-free, 593 
Dieulafoy aspirator, 49 
Digestive system, diseases of, 57 



Dilatation of esophagus, 65 
of stomach, acute, 76 
chronic, 77 

diagnosis, 78 
etiology, 77 
morbid anatomy, 77 
prognosis, 78 
symptoms, 77 
treatment, 78 
Dilatation of heart, 181, 209 
diagnosis, 211 
etiology, 209, 214 
morbid anatomy, 210 
physical signs, 210 
symptoms, 210 
treatment, 211 
Diphtheria, 355 

antitoxin in, 361 

complications and sequela of, 360 

diagnosis of, 360 

etiology of, 356 

intubation in, 365 

morbid anatomy of, 357 

prognosis of, 361 

prophylaxis in, 361 

symptoms, 358 

of laryngeal, 359 
of nasal, 359 
of pharyngeal, 358 
treatment of, \361 
Diphtheria antitoxin, 363 
Diphtheroid, 368 
Diplegia, infantile, 537 
Diplococcus, intracellularis, 524, 529 

pneumoniae, 18, 25 
Diplopia, 311, 513, 544 
Disinfection, 584 
in typhoid, 328 
of dejecta, 328 
of rooms, 584 
Distomatosis, 462 
hepatic, 463 
pulmonary, 463 
venal, 464 
Diverticulum of esophagus, 65 

Meckel's, 102 
Dracontiasis, 474 

Dropsy, from presence of aneurism, 236 

in anemia, 249 

in arteriosclerosis, 231 

in Bright's disease, 161 

in heart disease, 193 
Drunkenness, 296 

Duchenne-Erb type of lead palsy, 302 
Ductless glands, 246 
]:)uctus botalli, patent, 228 
7^um-dum fever, 4(5 1 
Duodenal ulcer, 89 
Dysentery, 93 

acute catarrhal, 93 

acute specific, 94 

amebic, 94 

chronic, 96 



602 



INDEX 



Dysentery, diphtheritic, 95 

following pneumonia, 25 
Dyspepsia, acute, 65 

chronic, 67 

nervous, 81 
Dysphagia in aneurism, 235 

in bulbar palsy, 511 

in disease of the esophagus, 63-65 

in laryngitis, 6, 7 

in myasthenia gravis, 311 
Dyspnea, cardiac, 192 

in abscess of lung, 38 

in aneurism, 235 

in asthma, 13 

in bronchopneumonia, 29 

in bulbar palsy, 311, 511 

in emphysema, 36 

in endocarditis, 192 

in lobar pneumonia, 21 

in myocarditis, 214 

in new growths of lung, 42 

in tuberculosis, 399 

in uremia, 157 

Ear, in diphtheria, 359 

in influenza, 338 

in measles, 354 

in Meniere's disease, 492 

in scarlet fever, 350 

in typhoid fever, 326 
Ebstein, 295 
Echinococcus cyst, 479 

fluid, 480 

booklets, 480 

multilocular, 480 
Edema, angioneurotic, 579 

from pressure of aneurism, 236 

in anemia, 249 

in arteriosclerosis, 231 

in Bright's disease, 161, 164, 167 

in heart disease, 193 

of larynx, 4 

of Imigs, 16, 26, 27 
Eel worms, 464 
Ehrlich's diazo reaction, 327 
Eighth nerve, 491 
Einthoven's electrocardiogram, 221 
Electrocardiogram, 221 
Elephantiasis, 473 
Eleventh nerve, 494 
Ellis line of dulness, 45 
Embolism in acute endocarditis, 187 

in chronic endocarditis, 201 

in phlebitis, 241 

of cerebral arteries, 25, 532 

of liver, 119 

of lung, 16 
Emphysema, atrophic, 37 

compensatory, 35 

hypertro]iliic, 35 

in pl(Mirisv with effusion, 46 

intorsliliah 37 
Empyema, diagnosis, 50 

etiology. 50 



Empyema following pneumonia, 24 

morbid anatomy, 50 

prognosis, 50 

treatment, 51 
Endocarditis, acute, 183 
simple, 184 

following pneumonia, 24 

following septicemia, 376 
Endocarditis, chronic, 187 

age in, 202 

arteries and kidneys in, 203 

complications of, 201 

eflfects of, 188 

etiology of, 187 

location of defect in, 202 

medicines in, 204 

morbid anatomy of, 188 

occupation in, 202 

physical methods in treatment of, 205 
baths, 205 
exercises, 205 
Oertel method in, 205 
Schott movements in, 205 
Zander methods in, 205 

prevention of, 203 

sequelae of, 192 

symptoms of, 192 

temperament in, 202 

treatment of, 203 
Endocarditis, malignant, see Septicemic, 
185 

Endocarditis, septicemic, 185 

diagnosis, 187 

etiology, 185 

morbid anatomy, 185 

symptoms, 185 

treatment, 187 
Enemata, cleansing, 586 

nutrient, 587 

therapeutic, 587 
Enteric fever, see Typhoid Fever, 313 
Enteritis, catarrhal, 83 

croupous, 85 

phlegmonous, 85 

ulcerative, 90 
Enteroclysis, 588 
Entero-colitis, 83 

etiology, 83 

morbid anatomy, 83 

prognosis, 84 

symptoms, 84 

treatment, 84 
Enteroliths, 103 
Enteroptosis, 109 
Eosinophilia. in asthma, 13 

in ta]ie-wonii infection, 478 

in trichiniasis, 4(58 

in uncinariasis. 470 
Ephemeral fever. 417 
Epididymis, tuberculosis of. 414 
Epiglottis, syphilis of, 444 

tubcvenlosis of, 5 
l>pilepsy, 555 

Jacksonian, 556 



INDEX 



603 



Epistaxis, 3 

Epithelioma, of esophagus, 65 

of intestine, li3 

of stomach, 73 
Erb's sign, 503 
Ergotism, 30(3 
Eructation, nervous, 82 
Eruption, antitoxin, 364 

in rlieumatic fever, 38 

of cerebrospinal meningitis, 527 

of glanders, 422 

of measles, 353 

of pellagra, 421 

of rotheln, 355 

of scarlet fever, 347 

of septicemia, 350 

of septic endocarditis, 186 

of small-pox, 453 

of syphilis, 442 

of trichiniasis, 468 

of typhoid fever, 322 

of tj^phus fever, 332 

of varicella, 458 
Erysipelas, 377 

complications, 378 

diagnosis, 378 

etiology, 377 

morbid anatomy, 377 

prognosis, 379 

symptoms, 377 

treatment, 379 
Erythroeytosis megalosplenica, 266 
Erythromelalgia, 578 
Esopliagitis, acute, 63 
Esophagus, cancer of, 65 

dilatation of, 65 

diverticulum of, 65 

spasm of, 63 

stenosis of, 64 

tuberculosis of, 392 

veins of, 63 
Estivo-autumnal fever, 437 
Estivo-autumnal parasite, 433 
Excretion, urinary, 152 

of chlorides, 159 

of other substances, 160 

of water, 159 
Exophthalmic goitre, 268 
Exophthalmos, 270 
Extrasystole, 220 

Exudate, in pleurisy with effusion. 

Facial nerve, 490 
Eacial paralysis, 490 
Eamine fever, 335 
Farcy, 421 

buds, 423 
Fastigiiim of typlioid, 320 
Febricula, 417 
Fecal impaction. 103 
Fehling's test. 286 
Fever, black-water, 440 

breakbone, 339 

cachexial, 438 



Fever, cerebrospinal, 524 

ephemeral, 417 

estivo-autumnal, 437 

famine, 335 

glandular, 419 

hay, 12 

hospital, 332 

hysterical, 568 

intermittent, 434 

jail, 332 

malarial, 429 

Malta, 344 

mountain, 420 

relapsing, 335 

remittent, 437 

Rocky Mountain, 420 

seven-day, 335 

ship, 332 

splenic, 425 

spotted, 332 

syphilitic, 442 

tick, 420 

typhoid, 313 

typho-malarial, 326 

typhus, 332 

yellow, 339 
Fibroid phthisis, 404 
Fifth nerve, 489 
Filaria Bancroft i, 471 
Filaria loa, 475 
Filariasis, 471 
Fingers, clubbed, 1 1 
Fish poisoning, 305 
Fistula in ano, 303 
Fits, epileptic, 555 
Flail leg, 507 
Flexner-Jobling serum, 529 
Flint murmur, 195 
Floating kidney, 151 

spleen, 263 
Fluid, ascitic, 148 

cerebrospinal, 529 

echinococcus, 480 

hydatid, 480 

pleural, 47 
Flukes, 462 
Food poisoning, 304 
Foramen ovale, patent, 228 
Fourth nerve. 488 
Friedliiiidei's bacillus, 19 
Friedlcbcii. 274 
Friedrcicirs ataxia, 517 
Fumigation, 584 

Gall-bladder, disi-ascs of. 131 
(Tall()i)iii,u coiisuitipt ion. 394 
rjall-sloncs. associated l(>si()ns of, 134 

l)iliaiy colic in. 135 

composition of. 134 

diai^nosis of, 136 

("tioh)gy of, 133 

in common duct, 135 

in cvsl ic duct, 135 

in gall-bladder, 134 



604 



INDEX 



Gall-stones in intestine, 103 
in papilla of Vater, 136 
leukocytosis in, 137 
morbid anatomy of, 133 
prognosis in, 137 
symptoms in, 134 
treatment of, 137 
Gangrene, in cerebrospinal fever, 528 
■ in diabetes. 28G 
in noma, 58 
of lung, 40 

hemoptysis in, 14 
Gastralgia, 81 
Gastritis, acute, 05 
chronic, 07 
croupous. 07 
parasitic, 07 
phlegmonous, 07 
toxic, 00 
chronic, 07 

and congestion, 192 
course of, 08 
diagnosis of, 08 
diet in, 08 
etiology of, 07 
lavage in, 09 
medicines in, 09 
morbid anatomy of, 07 
stomach contents in, OS 
symptoms of, 07 
treatment of, 08 
Gastrodynia, 81 
Gastroptosis, 78, 109 
Gastrorrhagia, 80 
Gastrosuccorrhea, 82 
Geographical tongue, 59 
German measles, 355 
Glanders, 421 

bronchial, 250, 397, 409 
cervical, 409 
diagnosis, 423 
etiologJ^ 421 
mediastinal. 250. 409 
mesenteric. 250, 409 
morbid anatomy, 422 
symptoms, 422 
treatment, 423 
Glands, parotid, 00 
salivary, 59 
see also Lymphadenitis 
Glandular fever, 419 
Glenard's disease, 109 
Glioma, of brain, 545 
Glossitis, acute, 59 
Glosso-labio-laryngeal paralvsis, 511 
Glossopharyngeal nerve. 492 
Glycogen. 285 
Glycosuria. 285 

in pancreatitis, 139, 140, 141 
Goitre, 207 

exophthalmic, 208 
course. 271 
diagnosis. 271 
etiology, 209 



Goitre, exophthalmic, morbid anatomy of, 
209 

symptoms, 209 
treatment, 271 
.Gonococcus, 142, 185, 383 
Gonorrheal arthritis, 383 
endocarditis, 385 
infection, 383 
I septicemia, 385 
, Gout, 280 

acute, 281 

associated lesions of, 280 

blood in, 280 

chemistiy of, 280 

chronic, 281 

diagnosis of, 282 

etiology of, 280 

irregular, 281 

joints in, 280 

morbid anatonn^ of, 280 

retrocedent, 282 

suppressed, 282 

treatment, 282 

urine in, 282 
Graefe's sign, 270 
Grain poisoning, 305 
Grand mal, 555 

Gravel, see Nephrolithiasis, 171 

Graves' disease, 208 

Green sickness, 240 

Grippe, 337 

Grocco's triangle, 45 

Guinea worm, 474 

Gumma, of brain, 545 

of cord, 522 

of liver, 444 

of spleen, 204 

HafFkine's serum, 344 
Hallucinations in delirium tremens, 298 
Hanot's disease, 124 
Hay fever, 2 

Headache, in brain tumor, 545 

in cerebral syphilis, 530, 545 

in hysteria, 500 

in neurasthenia, 572 

in typhoid fever, 317 

in uremia, 150 

sick, 558 
Head's zones, 99 
Heart-block, 220 
Heart, congenital defects of, 228 

degenerations of, 211 

dilatation of, 209 

diseases of, 183 

fatty, 213 

hyjiertrophy of, 208 

in ('m]ihysema. 36 

irregular. 210 

neuralgia of. 220 

neuroses of. 214 

palpitation of. 214 

rai)id (tachycardia). 215 

slow (biadyVardia). 210 



INDEX 



Heat exhaustion, 308 
Heberdens nodes, 27G 
Hemateuiesis, 81 
Hematomyelia, 502 
Hematuria, 152, 187 
Hemianopsia, 487, 535 
Hemiatrophy, facial, 579 
Hemiplegia, 534 

infantile, 537 
Hemoglobinuria, 153 

paroxysmal, 153 
Hemogiobinuric fever, 440 
Hemophilia, 257 

diagnosis, 258 

etiology, 257 

morbid anatomy, 257 

prognosis, 258 

symptoms, 258 

treatment, 258 
Hemoptysis, causes of, 14 
Hemorrhage, bronchopulmonary, 14 
in aneurism, 234, 235 
in chronic endocarditis, 201 
in infarction, 17 
in .pneumonia, 20 
in tuberculosis, 398 

cerebral, 533 

in arteriosclerosis, 231 
in nephritis, 167 

from hemorrhoids, 244 

from lungs, 14 

from nose, 3 

from pancreas, 138 

from stomach, 80 

gastric, 80 

in cirrhosis of liver, 121 
in gastric cancer, 74 
in gastric ulcer, 70 

in acute yellow atrophy, 117 

in cancer of stomach, 74 

in cirrhosis, 121 

in jaundice, 110 

in leukemia, 251 

in pernicious anemia, 249 

in purpura, 250 

in se])ticemia, 375 

in typhoid fever, 324 

in whooping-cough, 370 

in yellow fever, 340 

intestinal, in cancer, 114 
in duodenal ulcer, 90 
in typhoid fever, 324 
Hemorrhoids. 243 

etiology, 244 

prognosis. 244 

syiii])t()ins, 244 

treatment. 244 
Hemothorax, 52 
Henoch's disease, 250 
Hepatic circulation, disturbances of, 118 
Hepatitis, chronic, 120 
Hepatization of lung. 19 

signs of, 23 
Hernia, diaphragmatic, 56 

strangulated, 102 



Herpes labial is, in lobar pneumonia, 

in malaria, 435 

in meningitis, 527 

in relapsing fever, 330 
Herpes zoster, 501 
Hiccough, 490 
His, bundle of, 210 
Hobnail liver, 120 
Hodgkin's disease, 253 

course and prognosis, 254 

diagnosis, 254 

etiology, 253 

morbid anatomy, 253 

symptoms, 253 

treatment, 254 
Hooklets, echinococcus, 480 
Hospital fever, 332 
Hydatid disease, 479 
Hydrocephalus, 538 
Hydronephrosis, 173 
Hydropericardium, 182, 192 
Hydroperitoneum, 147, 192 
Hydrophobia, 423 

diagnosis, 424 

etiology, 423 

morbid anatomy, 423 

symptoms, 424 

treatment, 424 
Hydropneumothorax, 54 
Hydrothorax, 54, 192 
Hymenolepis nana, 470 
Hyperchlorhydria, 82 
Hyperesthesia, in hysteria, 500 

in myelitis, 504 

in neurasthenia, 572 

of stomach, 82 
Hyperglycemia, 285 
Hyperkinesis, 82 
Hyperorexia, 82 
Hypertrophy of heart, 181, 208 

of left ' ventricle, 208. 209 

of pylorus, 79 

of right ventricle, 193, 208, 209 

of thvnuis, 274 

of thyroid, 207 
Hypodermoclysis, 588 
Hypoglossal nerve. 495 
Hysteria, 505 

course and prognosis, 5()9 

diagnosis, 509 

etiology, 505 

symptoms, 505 

treatment, 570 

traumatic, 575 

Tee-coil, 592 

Icterus, s(>e Jaundic(\ 115 
IdiocN'. amaurotic family. 549 

llcocnlHis, 87 

Illuminating gas-poisoning, 307 
Tni])ac1 ion. fecal. 103 
Indicanuiia. 150 
Indigestion, acute, 05 
chionie, 07 



606 



INDEX 



Indigestion, intestinal, 86 

nervous, 81 
Inebriety, 296 
Infantile paralysis, 506 
Infarction, of heart, 211 
of kidney, 187 
of lung, 16 
of spleen, 187, 264 
Infection, gastro-enteric, 87 
Infections, bacterial, 185 
intestinal, 475 
visceral, 479 
Influenza, 337 

complications, 337 
course, 337 
diagnosis, 338 
etiology, 337 
morbid anatomy, 337 
prognosis, 338 
symptoms, 337 
treatment, 338 
Infusion, intravenous, 589 
Infusoria, 429 
Insolation, 308 
Insufficienc}^, aortic, 188, 195 
diagnosis, 197 
physical signs, 196 
prognosis, 197 
symptoms, 196 
mitral, 189, 193 
diagnosis, 194 
in aortic lesions, 189 
physical signs, 194 
prognosis, 194 
relative, 194 
symptoms, 193 
pulmonary, 199 
tricuspid, 200 
Intermittent fever. 434 
Intestines, cancer of, 113 
diseases of, 83 

hemorrhage from, in typhoid fever, 
324 

invagination of. 102 

neuroses of, 110 

obstruction of, 102 

stricture and tumors of, 102 

twists of, 102 
Intoxications, 296 
Intubation, 365 
Intussusception, 103 
Invagination, 102 
Island of Reil, 546 

Islands of Langerhans, in diabetes, 285 
Isolation, 583 

Jail fever, 332 
Jaundice, 115 

catarrhal, 131 

in cancer of liver, 127 

in cholelitliiasis, 135 

in pneumonia. 25 

in yellow fever, 340 

obstructive, 115 



Jaundice of new-born, 118 

toxemic, 116 
Joints, Charcot, 514 

flail, 507 

inflammation of, see Arthritis 

Kala-azar, 461 
Kaolinosis, 33 
Kernig's sign, 526 
Kidney, amyloid, 168 

anomalies of, 150 

congestion of, 152 

cystic, 169 

floating, 151 

gouty, 282 

horseshoe, 150 

movable, 151 

palpable, 151 

stone in, 171 

surgical, 170 

tests of functions of, 158 
tuberculosis of, 413 
tumors of, 174 
Kitasato, 343 

Klebs-Lofller bacillus, 58, 185, 305, 356 
Knots, of intestine, 102 
Koplik's spots, 353 

Laennec, metallic tinkle, 55 
Langerhans, islands of, 285 
Laryngismus stridulus, 5 
Laryngitis, acute, 3 

chronic, 4 

edematous, 4 

syphilitic, 6 

tuberculous, 5 
Larynx, ascaris in, 465 

diseases of, 3 

neuroses of, 6 

paralysis of, 494 

syphilis of, 6 

tuberculosis of. 5 
Lateral sclerosis, 516 
Lathyrism, 306 

Lavage of stomach, 69, 73, 75, 78 
Lead and chronic endocarditis, 188 
Lead poisoning, chronic, 301 
Leads of electrocardiogram, 221 
Leontiasis ossea, 311 
Lepra, 414 
Leprosy, 414 

diagnosis, 415 

etiology, 414 

morbid anatomy, 415 

prognosis. 415 

symptoms, 415 

treatment. 415 
Leptomeningitis, acute, 500 

cerebral, 523 

chronic. 500 

spinal. 500 
Leucin, in urine, 117 
Leukemia and hemoptysis, 14 

blood in, 251 



INDEX 



b07 



Leukemia, 249 

diagnosis, 252 

etiology, 250 

lymphatic, 252 

morbid anatomy, 250 

prognosis, 252 

splenomyelogenous, 250 

symptoms, 250 

treatment, 252 
Leukocytosis, in abscess of brain, 540 

in abscess of lung, 38 

in acute appendicitis, 100 

in acute meningitis, 529 

in acute rheumatic fever, 382 

in acute tuberculosis, 391, 395 

in cancer of intestines, 114 

in cholangitis, 137 

in cholecystitis, 137 

in chronic tuberculosis, 400 

in gout, 283 

in influenza, 338 

in intestinal obstruction, 106 

in lead poisoning, 312 

in leukemia, 251, 252 

in pericarditis, 179 

in peritonitis, 143 

in pleurisy, 43, 47, 51 

in pneumonia, 21 

in pyelitis, 171 

in Rocky Mountain spotted fever, 
420 

in septicemia, 375 

in septicemic endocarditis, 187 

in suppurative pancreatitis, 139 

in trichiniasis, 468 

in typhus, 334 
Leukopenia, in kala-azar, 461 

in miliary tuberculosis, 391 

in typhoid fever, 324 

in typhus fever, 334 
Leukoplakia buccalis, 59 
Lithuria, 154 
Little's disease, 538 
Liver, abscess of, 126 

acute yellow atrophy of, 116 

amyloid, 129 

anemia of, 118 

cancer of, 128 

congestion of, 118 

fattv, 128 

flukes, 463 

form and position of, 129 
hobnail, 120 
hyperemia, 118 
new growths of, 127 
nutmeg, 118 
sarcoma of, 128 
syphilis of, 444 
tuberculosis of, 393 
timiors of, 127 
Lobar pneumonia, 18 

blood in, 21 

complications of, 24 

diagnosis of, 25 



Lobar pneumonia, diplococcus of, 19 
etiology of, 18 
incubation of, 20 
morbid anatomy of, 19 
onset of, 20 
physical signs of, 22 
prognosis of, 20 
serum in, 27 
special forms of, 23 
treatment of, 26 
Lobular pneumonia, 28 
Lockjaw, 416 
Locomotor ataxia, 512 
Long thoracic nerve, 497 
Lues, see Syphilis, 441 
Lungs, abscess of, 24, 37 
cirrhosis of, 24, 32 
congestion, active, 15 
congestion, passive, 15 
diseases of, 15 
edema of, 16 
gangrene of, 24, 40 
hyperemia of, 15 
hypostatic congestion of, 15 
induration of, 24, 32 
new growths of, 41 
syphilis of, 444 
tuberculosis of, 394 
Lustig and Galleotti, treatment of 

plague, 344 
Lymphadenitis in diphtheria, 358, 360 
in glandular fever, 419 
in scarlet fever, 349, 350 
in syphilis, 443 
tubercular, 409 
Lymphatic leukemia, 252 
Lymphatism, 262 
Lyssa, 423 

McBurney's point, 98 
Main en griflfe, 497 
Malaria, 429 

diflferentiation of, 187 
^Malarial fever, 429 

etiology, 429 

morbid anatomy, 433 

prognosis, 439 

s,\nuptoms, 434 

treatment, 439 
Malignant endocarditis, see Endocardi- 
tis, sei)ticeniic. 185 
^Malignant pustule, 425 
Malta fever, 344 

Marie's hereditary cerebellar ataxia, 516 
Mastigophora, 429 
Measles. 352 

complications and sequelae, 354 

d('s(]ii;niiat ion, 354 

diagnosis. 354 

eruption. 353 

etiology. 352 

German. 355 

invasion. 353 

morbid anatomy, 353 



608 



INDEX 



Measles, prognosis, 354 
symptoms, 353 

treatment, 354 
Meat measles, 467 
Median nerve, 497 
Mediterranean fever, 344 
Medulla, tumors of, 546 
INIegrim, 558 
Membranous croup, 359 
Meniere's disease, 492 
Meninges, diseases of, 523 
Meningism, 529 
Meningitis, acute, 524 

cerebrospinal, 524 

differentiation of, 529 

following abscess of brain, 540 

following pneumonia, 25 

serous, 298 

suppurative, 525 

syphilitic, 530 

tuljerculous, 525 
Menstruation, vicarious, 14 
Micrococcus lanceolatus, 18 

melitensis, 344 
Migraine, 558 
Miliary fever, 419 
Milk sickness, 419 
Mitchell (Weir) rest cure, 574 
Mitral insufficiency, 189, 193 

stenosis, 190, 'l94 
Mobius' sign, 271 
Morbilli, 352 

Morbus maculosus neonatorum, 259 

Morphine habit, 299 

Morphinism, 299 

Mosquito, in yellow fever, 340 

malarial, 430 
Moulds, 428 
Mouth, care of, 586 

diseases of, 57 
Mucous patches, 443 
Mueller, muscle of, 270 
Mumps, 371 

Murmurs, accidental, 194 
hemic, 194 
in aneurism, 234 
in aortic insufficiency, 197 
in aortic stenosis, 198 
in mitral insufficiency, 193 
in mitral stenosis, 195 
in pulmonary stenosis. 199 
in tricuspid insufficiency, 200 
in tricuspid stenosis, 201 
in myocarditis. 212. 214 
pericardial, 177 
pleuropericardial, 177 

Muscarin, 306 

]\Tnselos. diseases of. 309 

Muscnlospiral nerve, 497 

Mushrooms. 305 

Myalgin, 279 

Mynstlionia ,-^ra\ is. 31 1 

Mycosis intosi iiialis. 426 

Myelitis, coni])ressi()ii. ,"05 



Myelitis, general, 503 

transverse, 503 
Myelocytes, in leukemia, 251 
Myocarditis, acute, 212 
etiology, 212 
morbid anatomy, 212 
prognosis, 212 
symptoms, 212 
treatment, 213 
chronic, 213 

etiology, 213 
morbid anatomy, 213 
symptoms, 214 
treatment, 214 
Myocardium, in chronic endocarditis, 
188, 191, 201 
degeneration of, 212 
Myositis ossificans, 310 

suppurative, 308 
Myotonia, congenital, 310 
Mytilotoxicon, 305 
Myxedema, 271, 272 
operative, 271 

Nauheim baths, 205 
Nematoda, 462 
Nephritis, acute, 160 
diagnosis, 161 
etiology, 160 
in pneumonia, 25 
in scarlet fever, 350 
in typhoid fever, 326 
morbid anatomy, 160 
symptoms, 161 
treatment, 101 
Nephritis, chronic, 162 

and arteriosclerosis, 231 
and endocarditis, 188, 191 
Nephritis, chronic interstitial. 165 
diagnosis of, 165 
etiology of. 165 
morbid anatomy of, 165 
prognosis of, 167 
symptoms of, 166 
treatment of, 167 
Nephritis, chronic, parenchymatous. 163 
course and prognosis of, 
164 

etiology of. 163 
morbid anatomy of. 163 
symptoms. KJo 
treatment, 164 
Nephrolithiasis. 171 
diagnosis of. 172 
etiology. 171 
morbid anatomy of. 171 
prognosis of. 172 
symjitoms of. 172 
treatment of. 172 
Ne])liroptosis. 151 
N('p]iroty]dioid. 319 
N.'rvos. 'eorol)rnl. -!S5 
jieripliernl. 482 
spinal. -196 



INDEX 



609 



Nen'es, diseases of, 482 
Neuralgia, 559 

intercostal^ 560 
lumbar, 561 
of heart, 226 
of lower extremity, 561 
of upper extremity, 561 
trigeminal, 560 
red, 578 
Neurasthenia, 570 
course, 573 
diagnosis, 573 
etiology, 571 
prognosis, 573 
symptoms, 571 
treatment, 574 
Neurasthenia, traumatic, 575 
Neuritis, 482 
acute, 483 
alcoholic, 297, 483 
arsenical, 303, 483 
in beri-beri, 345 
in diabetes, 286 
in diphtheria, 360 
in erysipelas, 278 
in pneumonia, 25 
in typhoid fever, 326 
localized, 482 
multiple, 483 
optic, 486 
primary, 483 
secondary, 483 
Neuromata, 484 
multiple, 484 
solitary, 484 
Neuroses, 549 

occupational, 564 
of esophagus, 63 
of heart, 214 
of intestine, 110 
of larynx, (i 
of stomach, 81 
traumatic, 575 
New growths, of brain, 544 
of cord, 522 
of esophagus, 65 
of intestine, 102, 113 
of kidncv, 174 
of liver," 127 
of lung, 41 
of pinioions, 140 
of |)cric;n<lium, 182 
of peritoneum, 147 
of spleen, 264 
of stomach, 73 
of thymus, 274 
of thyroid, 268 
Night sweats, in tuberculosis, 300 

treatment of, 408 
Nocardia, 427 
Nodes, Heberden's, 276 
Nodules, subcutaneous rheumatic, 382 
Nicoll, 274 
Ninth nerve, 402 



Noma, 58 

Nose, diseases of, 1 
Nose-bleeding, 3 
Nutmeg liver, 118 
Nystagmus, 489 

Obermeiei'. spirillum of, 335 
Obesity, 294 

diet in, 295 
etiology, 294 
metabolism in, 294 
morbid anatomy, 204 
symptoms, 295 
treatment, 295 
Obstipation, 107 
Obstruction, intestinal, 102 
diagnosis, 105 
etiology, 102 
prognosis, 106 
symptoms, 104 
treatment, 106 
pyloric, 71 
Oculomotor nerve, 488 
Oertel's method, in chronic endocarditis, 

206 
Oidia, 428 

Olfactory nerve, 485 
Opium poisoning, 290 
Optic nerve and tract, 486 

atrophy of, 487 

neuritis of, 487 
Organothera])y in Addison's disease, 202 
in Graves" disease, 271 
in myxedema, 274 
Orthodiagram, 207 
Osteitis deformans, 312 
Osteoarthropathy, In^pertrophic pul- 
monary. 312 
Otitis media, in diphtheria, 359 

in influenza, .')38 

in measles, .'354 

in pneumonia, 25 

in scarlet fever, 350 

in typhoid fever, 326 

thrombosis in, 531 
Oxaluria, 155 
Oxybutyric acid, 288 
Oxyuriasis, 465 
Oxyuris, 465 

Pachymeningitis, cerebral, 523 
external, 523 
internal, 523 
spinal, 499 
Packs, cold. 591 
dry. 5!)0 
wet, 5!)0 
Paget's disease, 311 
I'a inters' colic. 301 
l'all)itation of heart, 214 
etiology. 214 
physical signs. 215 
symptoms, 211 
treat nienl, 215 



610 



INDEX 



Pancreas, calculi of, 141 

carcinoma of, 140 

cysts of, 140 

diseases of, 137 

in diabetes, 284 

tumors of, 140 
Pancreatitis, acute, 137 

hemorrhagic, 137 

chronic, 139 

gangrenous, 138 

suppurative, 137 
Papillitis, 487 

Paracentesis of abdomen, 149 

of chest, 49 
Paragonimus, 463 
Paralysis, acute ascending, 508 

agitans, 550 

brachial, 497 

bulbar, 511 

diphtheritic, 360 

facial, 490 

family periodic, 576 

glosso-labio-laryngeal, 511 

hereditary spastic spinal, 510 

hysterical, 569 

infantile cerebral, 537 

infantile spinal, 506 

in meningitis, 528 

in syringomyelia, 519 

Landry's, 508 

laryngeal, 493 

lead, 301 

nuclear, 490 

of cerebral nerves, 485 

of spinal nerves, 496 

periodic, 576 

peripheral, 490 

pharyngeal, 493 

progressive, 541 
bulbar, 511 

spastic spinal, 515 

supranuclear, 490 
Paralytic stroke, 533 
Paramyoclonus multiplex, 311 
Paraphasia, 548 
Paraplegia, 517 

ataxic. 517 

hysterical, 568 

spastic, 515 
Parasites, animal, 429 

estivo-autumnal, 433 

quartan, 433 

tertian, 432 
Parathyroid, 550, 563 
Paresis, general, 540 
Parotitis, acute, 59 

chronic. 60 

epidemic, 371 

in pneumonia, 25 
Paste-mustard, 591 
Peliosis rlu'umatica, 256 
Pellagra. 306. 420 
Perforation, in a])])endicitis, 97 

ill duodenal ulcer, 90 



Perforation, in gastric ulcer, 81 

in typhoid fever, 325 
Pericarditis, acute, 175 

bacteriology, 175 

blood in, 179 

course and prognosis, 179 

diagnosis, 180 

etiology, 175 

morbid anatomy, 175 

physical signs, 177 

symptoms, 176 

treatment, 180 
acute fibrinous, 175 
cancerous, 182 
chronic adhesive, 181 
hemorrhagic, 180 
in acute rheumatic fever, 381 
in influenza, 338 
in pneumonia, 25 
in scarlet fever, 350 
in typhoid fever, 325 
purulent, 180 
serous, 177, 211 
tubercular, 182 
with effusion, 177, 211 
Pericardium, adherent, 177 

diseases of, 175 
Peritoneum, cancer of, 147 
diseases of, 142 
fluid in ascites, 148 
tuberculosis of, 411 
Peritonitis, acute general, 142 
appendical, 99 
chronic, 146 

chronic hemorrhagic, 146 

general adhesive, 146 

in cholecystitis, 133 

in duodenal ulcer, 90 

in gastric cancer, 75 

in gastric ulcer, 71 

in pancreatitis, 139 

in typhoid fever, 325 

local adhesive, 146 

pelvic, 145 

proliferative, 14(5 

subphrenic, 145 

tubercular, 411 
Pernicious anemia, 247 
Pel-tussis, 369 
Pest, 343 
Pestis major, 343 

minor, 343 

siderans. 343 
Petechi.T. 255 
Petit mal, 556 
Pfeifter, bacillus of. 337 
Pliaryngeal diptheria. 358 
Phar^mgitis, acute catarrhal, 60 

chronic. 60 

granular. 60 

sicca. 60 
Pharynx, diseases of. 60 

])aralvsi8 of. 493 
Phlebitis." acute. 23!) 



INDEX 



Phlebitis, effects of, 239 

etiology, 239 

morbid anatomy, 239 

of appendicular veins, 241 

of femoral vein, 241 

of jugular vein, 241 

special varieties of, 241 

symptoms, 240 

treatment of, 242 
Phlegmonous enteritis, 85 

gastritis, G7 
Pliosphaturia, 155 
Phrenic nerve, 49G 
Phthisis, acute pneumonic, 394 

chronic ulcerative, 39G 

fibroid, 404 
Pick's disease, 412 

Pigmentation in Addison's disease, 203 

in arsenical poisoning, 304 
Piles, 243 
Pin-worms, 4G5 
Plague, 342 

bubonic, 342 

diagnosis, 344 
etiology, 342 
morbid anatomy, 343 
prognosis, 344 
symptoms, 343 
treatment, 344 
Plasmodium malariae, 431 
Pleura, disease of, 42 
paracentesis of, 49 
tuberculosis of, 410 
Pleurisy, acute, 42 
chronic, 53 
diaphragmatic, 52 
dry, 42 
fibrinous, 42 
fluid in, 47 
hemorrhagic, 52 
in pneumonia, 24 
in tuberculosis, 410 
pulsating, 51 
purulent, 50 
sacculated, 50 
serous, 43 

special forms of, 52 

treatment of, 48 

tul)eicular, 410 

^y\th effusion, 43 
Plcuropeiicnrdial murmurs, 177 
Plexus i)rachial, 497 

cixical. 49G 

lumbar, 498 

sacral, 498 
Pluml)ism, 301 

Pneumococcus, 18, 48, 50, 133, 185, 389, 
529 

Pneumogastric neive, 493 
Pneuuiocoii iosis, 33 
Pneumonia, 18 

aspiration, 28 

asthenic, 24 

broncho, 28 



Pneumonia, caseous, 394 
central, 23 
cerebral, 24 
creeping, 24 
croupous, 18 
double, 23 
librinous, 18 
fibrous, 32 

in acute rheumatic fever, 382 

in cerebrospinal fever, 528 

in diphtheria, 3G0 

in erysipelas, 378 

in influenza, 337 

in measles, 354 

in plague, 344 

in scarlet fever, 350 

in small-pox, 455 

in typhoid fever, 326 

in whooping-cough, 370 

interstitial, 32 

larval, 24 

lobar, 18 

complications of, 24 
diagnosis of, 25 
etiology of, 18 
hemoptysis in, 14 
morbid anatomy of, 19 
physical signs of, 22 
prognosis oi, 26 
symptoms of, 20 
treatment of, 26 
lobular, 28 
massive, 23 
terminal, 24 
toxic, 24 
secondary, 24 
Pneumopericardium, 182 
Pneumothorax, 54 
Podagra, see Gout, 280 
Poliomyelitis, acute antei ior, 506 

chronic anterior, 509 
Polyarthritis, clironic, 275 
diagnosis, 277 
etiology, 275 
morbid anatomy, 275 
prognosis, 278 
symptoms, 276 
.treatment, 278 
Polycvtlioin ia. 2()() 
PolytuM-.ril is. 4S;; 
Polyserositis, chronic, 412 
Pons, tumors of, 546 
Porencephalus, 537 
Pork, in 1 1'icliiniasis, 4(i7 

taj)e-worm, 47() 
l^oital vein, embolism or thrombosis 
1 19 

stenosis of, 119 
Potain aanirator, 49 
Poultice, (laxseed, 591 
Progressive bulbar paralysis, 511 
Protozoa, pathogenic, 429 
Protozoan diseases, 42!) 



612 



INDEX 



Pruritus in jaundice, 116 

in diabetes, 289 
Pseudo-angina, 227 
Pseudo-diplitlicria, 3GS 
PseudoleuKeniia, see Hodgldn's disease, 
253 

Ptomaine poisoning, 305 
Ptosis, 48y, 535 
Ptyalism, 59 
Pulsation, capillary, 197 

expansile in aneurism, 237 
Pulse, alternating, 220 

arrhythmia of, 216 

capillary, 197 

Corrigan, 197 

delayed, in aneurism, 235 

extrasystolic in, 220 

heart-block in, 220 

in aortic insuthciency, 197 

in aortic stenosis, 198 

in mitral insufficiency, 194 

in mitral stenosis, 194 

in j)ericarditis with effusion, 177 

in jDneumonia, 21 

in typhoid fever, 321 

paradoxical, 177 

perpetually irregular, 220 

rapid, 215 

respiratory variations in, 220 

slow, 216 

venous, 200 

water-hammer, 197 
Pulsus alternans, 220 

paradoxus, 177 
Puncture, lumbar, 529 
Pupils, 488 

Argyll-Robertson, 489 
Purpura and hemoptysis, 14 
hemorrhagica, 256 
rheumatica, 256 
simplex, 255 
Pyelitis. 170 

bacteriology, 170 

etiology, 170 

morbid anatomy, 170 

symptoms, 170 

treatment, 171 
Pyelonephritis, 170 
Pyemia, 376 

Pylephlebitis, suppurative. 119 
Pylorus, congenital stenosis of, 79 

insufficiency of, 83 

spasm of, 83 
Pyonephrosis, 170 
Pyopneumothorax, 54 
Pyuria, 154 

Quartan fever, 434 

parasite. 433 
Quincke's disease, 579 
Quinsy. 62 

Quotidian intermittent fever, 434 
Rabies, 423 



Rachitis, 290 

course and prognosis, 292 

diagnosis, 292 

etiology, 290 

morbid anatomy, 291 

skeleton in, 292 

symjDtoms, 291 

treatment, 292 
Radiograms of esophagus, 64 

of lungs, 39, 42 

of pleura, 47 

of stomach, 78, 110 
Rales in asthma, 13 

in bronchiectasis, 11 

in bronchitis, 8, 9 

in bronchopneumonia, 30 

in congestion of lungs, 15 

in edema of lungs, 16 

in infarction of lungs, 17 

in lobar pneumonia, 23 

in pleurisy, 43, 46 

in pneumothorax, 55 
Rashes, antitoxin, 364 

of cerebrospinal meningitis, 527 

of glanders, 422 

of measles, 353 

of pellagra, 421 

of rheumatic fever, 381 

of rotheln, 355 

of scarlet fever, 347 

of septicemia, 350 

of septicemic endocarditis, 186 

of small-pox, 453 

of syphilis, 442 

of trichiniasis, 468 

of typhoid fever, 322 

of typhus fever, 332 

of varicella, 458 
Raynaud's disease, 577 
Reaction, Calmette, 403 

Ehrlich's diazo, 327 

of degeneration, 483 

von Pirquet's, 402 

Wassermann, 447 

Widal, 327 
Reflexes, Babinski, 504, 505 

deep, 504, 505, 512 

patellar, 504, 505, 512 
Reil, island of, 546 
Relapsing fever, 335 

complications, 336 
diagnosis, 336 
etiology, 335 
morbid anatomy, 335 
symptoms, 335 
treatment, 337 
Recurring fever, 335 
Remittent fever, 437 
Resolution of lung, 19 
delayed, 23 
signs of. 23 
Retinitis, 486 
Retzius, veins of, 121 
Retropharyngeal abscess, 60 



INDEX 



613 



Rheumatic fever, acute, 379 

and endocarditis, 187 

bacteriology of, 380 

comi^lications of, 381 

diagnosis of, 382 

etiology of, 379 

morbid anatomy of, 380 

prognosis of, 382 

treatment of, 382 
Eheumatism, chronic, see Polyarthritis, 
275 

gonorrheal, 383 
muscular, 279 

Rhinitis, acute, 1 

Rice-water stools, 91 

Rickets, see Rachitis, 290 

Risus sardonicus, 416 

Rocky Mountain spotted fever, 420 

Roentgen rays, in abscess of lung, 39 
in aneurism, 237 
in exophthalmic goitre, 271 
in Plodgkin's disease, 254 
in leukemia, 252 
in new growths of lung, 41 
in polycythemia, 267 
in pulmonary tuberculosis, 403 
in splenic anemia, 265 

Rotheln, 355 

Round-worms, 464 

Rubella, 355 

Rubeola, 352 

Rumination, 83 

Saccharomyces albicans, 58 
Sacral plexus, 498 
St. Vitus' dance, 551 
Salivation, 59 

Salivary glands, diseases of, 59 
Salvarsan, 450 
Sapremia, 374 
Sarcodinia, 429 
Sarcoma, of kidney, 174 
of liver, 127 
of lung, 41 
Saturnism, 301 
Scanning speech, 544 
Scarlatina, 340 
Scarlet fever, 346 

and endocarditis, 187 

anginose form of, 349 

clinical types of, 348 

complications and sequelae of, 
350 

desquamation of, 348 

diagnosis of, 350 

eruption of, 347 

etiology of, 347 

morbid anatomy of, 347 

prognosis of, 351 

prophylaxis of, 351 

symptoms of, 348 

treatment of, 351 
Schonlein's disease, 256 
Schott movements, 206 



Sciatica, 498 

Scleroderma, 580 

Scolices of ecliinococcus, 480 

Scrofula, 409 

Sclerosis, disseminated, 543 

insular, 543 

lateral, 515 

multiple, 543 

of heart, 211 

of liver, 120 

of lung, 32 

posterior spinal, 512 
Scorbutus, 259 
Scurvy, 259 

course, 260 

diagnosis, 260 

etiology, 259 

morbid anatomy, 259 

sjnnptoms, 259 

treatment, 260 
Scurvy and hemoptysis, 14 
Scurvy, infantile, 260 
Septic intoxication, 374 
Septicemia, 374 

gonorrheal, 185 

uterine, 185 
Septico-pyemia, 374 
Serum, Haffkine's, 344 

in diphtheria, 363 

in hemophilia, 258 

in meningitis, 531 

in pneumonia, 27 

in purpura, 257 

in septicemic endocarditis, 187 

in tetanus, 417 

Yersin's, 344 
Seven-day fever, 335 
Seventh nerve, 490 
Shiga bacillus, 94 
Shingles, 561 

Ship fever, see Typhus Fever, 332 

Sick headache, 558 

Sick-room, 582 

Siderosis, 33 

Sinus thrombosis. 531 

Siriasis 308 

Sixth nerve, 489 

Skodaic resonance, 23, 45 

Small-pox. 451 

complications. 455 

diagnosis. 456 

distribution, 451 

etiology, 451 

morbid anatomy, 452 

prognosis, 456 

symptoms, 452 

treatment, 456 
Southey's tubes, 162 
Spasm, of cardia. 83 

of csopliagns, 63 

of pylorus. 83 
Spasms, professional, 564 
Spastic spinal paralysis, 515 
hereditary, 516 



614 



INDEX 



SiDeech, scanning, 544 
Sphygmograpli, 219 
Sphygmomanometer, 206 
Spinal accessory nerve, 494 
cord, circulation of, 501 
comf>ression of, 505 
diseases of, 499 
hemorrhage into, 502 
meninges of, 499 
tumors of, 522 
nerves, diseases of, 496 
paralysis, infantile, 506 

spastic, 522 
sclerosis, posterior, 512 
Spirillum Obermeieri, 335 

of syphilis, 447 
Spirocheta pallida, 447 
Spleen, abscess of, 264 
amyloid, 264 
carcinoma of, 264 
cysts, echinococcus, 264 
diseases of, 263 
in cirrhosis, 123 
in failing compensation, 192 
in leukemia, 252 
in malaria, 435 
in pseudo-leukemia, 254 
in typhoid fever, 316 
infarct of, 264 
movable, 263 
rupture of, 263 
tumors of, 264 
Splenic fever, 425 
Splenomegly, 264 
tropical, 461 
Spotted fever, 332, 524 
Staphylococcus, 28, 50, 133, 143, 185, 

375, 389, 529 
Status epilepticus, 556 

lymphaticus, 262 
Stegomyia fasciata, 341 
Stelhvag's sign, 270 
Stenosis, aortic, 190, 198 
diagnosis, 198 
physical signs, 198 
prognosis, 197 
symptoms, 198 
mitral, 190, 194 
diagnosis, 195 
physical signs, 194 
prognosis, 195 
symptoms, 194 
pulmonary, 199 
diagnosis, 200 
prognosis, 200 
symptoms, 199 
Sputum, albuminous after aspiration, 50 
in acute bronchitis, 8 
in acute tuberculosis, 386, 394 
in bronchial asthma, 13 
in bi'oucliiectasis, 11 
in chronic bronchitis". 9 
in chronic tuberculosis, 398 
in gangrene of lung, 40 



Sputum, in lobar pneumonia, 20 
in pneumoconiosis, 34 
in pulmonary abscess, 38 
in pulmonary congestion, 192 
in pulmonary infarction, 17 

Stenson's duct, 59 

Steppage gait, 483 

Stercoral ulcer, 90 

Sternberg's treatment of vellow fever, 
342 

Stigmata of hysteria, mental, 566 
motor, 506 
sensory, 566 
Stokes-Adams syndrome, 214, 224 
Stomach, atrophy of, 67 

cancer of, 73 

contents, 68, 71, 74, 77 

dilated, 56 

diseases of, 65 

hemorrhage from, 80 

neuroses of, 81 

sclerosis of, 67 

ulcer of, 69 
Stomatitis, catarrhal, 57 

gangrenous, 58 

herpetic, 57 

parasitic, 58 

ulcerative, 57 
Stone, in kidney, 171 
Stools, disinfection of, 328 

in cholera, 91 

in cholera infantum, 87 

in cholera nostras, 85 

in dysentery, 93 

in enteritis, 84 

in gastro-enteric infection, 87 

in ileo-colitis, 88 

in intestinal indigestion, 86 

in intestinal ulceration, 89 

in intussusception, 104 
Strangulation of bowel, 102 
Strawberry tongue, 348 
Streptococcus, erysipelatis, 377 

mitior, 185 

pvogenes, 28, 58, 133, 143, 375, 389, 
^529 

rlieumaticus, 380 

viridans, 185 
Stricture of esophagus, 04 

of intestine, 102 
St. Vitus' dance, 552 
Subacidity, 82 
Succussion, 55 

Sudamina in acute rheumatic fever, 380 
Sugar in urine, in diabetes, 285 

in pancreatitis, 139, 140, 
141 

SuG'gestibilitv. 567 

Sunstroke, 308 

Super-Secret ion. 82 

Sweat iiiu' in triehiniasis, 468 

in tuberculosis. 390. 394, 399 

in typhoid fever, 326 

sickness, 419 



INDEX 



Sydenham's chorea, 551 
Syphilis, acquired, 442 

diagnosis of, 446 

etiology of, 441 

hereditary, 445 

of digestive system, 443 

of genito-urinary system, 444 

of respiratory system, 444 

of vascular system, 444 

prognosis of, 449 

prophylaxis of, 449 

spirochete of, 441 

treatment of, 450 

\Yassermann reaction in, 447 
Syringomyelia, 518 

course, 519 

diagnosis, 519 

etiology, 518 

morbid anatomy, 518 

prognosis, 522 

symptom^, 519 

treatment, 522 

Tabes dorsalis, 512 
Tachycardia, 201, 215 

etiology, 215 

paroxysmal, 221 

treatment, 215 
Tache cerebrale, 527 
Tenia echinococcus, 479 

mediocanellata, 475 

solium, 470 
Tentn nerve, 493 
Tetanilla, 562 
Tetanus, 410 

diagnosis, 417 

etiology, 416 

morbid anatomy, 416 

prognosis, 417 

symptoms, 416 

treatment, 417 
Tetany, 562 
Thermic fever, 308 
Third nerve, 488 
Thomsen's disease, 310 
Thrill, presvstolic, 193, 195 

systolic. 193, 198, 199 
Thronibokinase, 258 
Thrombosis, etiology of, 242 

of cerebral arteries, 25, 532 

of cerebral sinuses, 531 

of liver, 119 

of lung, 16 

special types of, 243 

svniptonis of, 243 
Thrush, r,S 

Thvmus gland, diseases of, 274 
Thyroid gland, 267 

acute inflammation of, 267 

congestion of. 267 

goitre. 267 

tumors of. 268 
Thyroiditis. 267 
Tic douloureux, 560 



I Tick fever, 420 

I Tinnitus, 491 

j Tongue, care of, 586 

diseases of, 57 

eczema of, 59 

geographical, 59 

in acute gastritis, 66 

in scarlet fever, 348 

in typhoid fever, 3 18-, 322 
Tonsillitis, acute follicular, 61 

chronic, 62 

suppurative, 62 
Tophi, in gout, 280 
Torticollis, acquired, 495 

congenital, 495 

spasmodic, 495 
Towns-Lambert treatment, 300 
of alcoholism, 297 
of cocaine habit, 301 
of opium habit, 300 
Tracheal tug, in aneurism, 235 
Tracheotomy in diphtheria, 365 
Transfusion in hemophilia, 258 

in purpura, 257 

in septicemic endocarditis, 1 
Traube's space, 45 
Traumatic neuroses, 575 
Trematoda, 462 
Tremor, in alcoholism, 297 

in exoplithalmic goitre, 271 

in multiple sclerosis, 543 

in paralysis agitans, 550 
Trichina^, 466 
Trichinella spiralis, 466 
Trichiniasis, 466 
Trichomonas intestinalis, 462 

vaginalis, 462 
Trigeminus nerve, 489 
Trismus, 416, 489 
Trochlear nerve, 488 
Trousseau's sign, 563 
Trypanosomes, 459 
Trypanosomiasis, 459 
Tubercle, miliary, 388 

solitary, of brain. 545 
Tubercula dolorosa, 485 
Tuberculin, diagnostic use of, 40 

therapeutic use of, 408 
Tumors, of brain, 544 

of cord, 522 

of esophagus, 65 

of inlesline. 102 

of kidney, 174 

of li\('r. 127 

of lung, 41 

of pancreas. 140 

of pericardium, 182 

of peritoneum. 147 

of spleen. 2(54 

of stomach, 73 

of thvmus, 274 

of thyroid. 268 
Twelfth nerve, 495 



616 



INDEX 



Twists and knots of bowel, 102 
Tubeiciilosis, 38-5 

acute miliary, 389 

general type, 390 
meningeal type, 390 
pulmonary type, 390 
acute pneumonic, 394 

broncliopneumonic type, 394 
lobar pneumonic type, 394 
age in, 388 
bacillus of, 385 
bovine infection in, 387 
" by ingestion, 387 
by inlialation, 386 
by inoculation, 388 
chronic pulmonary, 396 
constitution in, 388 
diagnosis of, 402 
differentiation of, 187 
distribution of, 385 
environment in, 388 
from meat, 387 
from milk, 387 
general, 389 

general treatment of, 405 

hemorrhage in, 14 

heredity in, 386, 388 

in diabetes, 286 

in measles, 354 

in pleurisy, 410 

in whooping-cough, 370 

modes of infection in, 386 

of circulatory system, 409 

of digestive system, 391 

of epiglottis, 5 

of esophagus, 392 

of female generative organs, 414 

of Fallopian tubes, 414 

of uterus, 414 
of genito-urinary system, 413 

of bladder, 413 

of testicle, 413 
of intestines, 392 
of kidney, 413 
of larjTix, 5 
of liver, 393 
of lungs, 394, 396 
of lymph-nodes, 409 

bronchial, 410 

cervical, 409 

general, 410 

mesenteric, 410 
of nervous -system. 414 
of pericardium, 411 
of peritoneum, 411 
of pleura, 410 
of respiratory system, 393 
of serous membranes, 410 
of spleen, 264 
of vocal cords, 5 
physical signs of, 400 
predisposing causes of, 388 
prognosis of. 403 
-prophylaxis of, 405 



Tuberculosis, race in, 388 
sex in, 388 

sources of infection in, 386 
treatment of, 405 

air and climate, 406 

diet, 407 

drugs, 407 

hygiene, 407 

tuberculin, 408 
Tufnell's diet, 238 
Typhoid bacillus, 305 

carriers, 314 

in cholecystitis, 133 

in endocarditis, 185 

in i^leurisj", 42 

in pneumonia, 19 
Typhoid fever, 313 

abortive, 319 

afebrile, 320 

age in, 313 

ambulatory, 319 

and malaria, 326 

bacteriology of, 313 

baths in, 330 

bed sores, 326 

blood in, 324 

blood-vessels in, 317 

boils, 326 

cause of death, 327 
cerebral symptoms, 323 
chills in, 321 

circulatory failure in, 331 
complications of, 324 
convalescence in, 318 
cultures in, 327 
defervescence in, 320 
diagnosis of, 326 
diarrhea in, 322 
dicrotism of pulse in, 321 
diet in, 329 

Ehrlich's diazo reaction, 327 
eruption of, 322 
fastigium of, 320 
general course of, 317 
heart in, 316 
hemorrliage in, 324 
hemorrhagic, 319 
hydrotherapy in, 329 
immunity from, 313 
in aged, 319 
in children, 319 
incubation of, 317 
inoculations, preventive in, 328 
insanity following, 326 
intestines in, 314 
kidneys in, 317 
laryngitis in. 326 
lobar jineumonia in, 326 
lungs in. 317 
lymiih-nodes in, 316 
malignant. 319 
management of. 328 
medicines in. 329 
muscles in, 317 



INDEX 



617 



Typhoid fever, neuritis in, 326 
otitis media in, 326 
parotitis in, 325 
perforation in, 325 
periods of, 317 
periostitis in, 326 
pleurisy, 326 

preventive inoculations in, 328 

prognosis, 327 

prophylaxis, 328 

protracted, 319 

pulse in, 321 

recrudescences of, 321 

relapse in, 321 

season in, 313 

spine in, 326 

spleen in, 316, 323 

susceptibility to, 313 

temperature in, 320 

tenderness in, 322 

thrombosis in, 325 

tongue in, 322 

transmission of, 314 

treatment of, 328 

tympanites in, 322 

urine in, 324 

Widal reaction in, 327 

without intestinal lesions, 316 
spine, 326 
state, in cholera, 91 

in septicemia, 375 
type, miliary tuberculosis, 390 
Typhomania, 549 
Typhus abdominalis, 313 
exanthematicus, 332 
Typhus fever, 332 
Tyrotoxicon, 305 
Tyrossin, in urine, 117 

Ulcer, duodenal, 89 

follicular, 88, 90 

intestinal, 89 

of intestines, 89 

of mouth, 57 

of stomach, 69 

peptic, 69 

rectal, 114 

round, 69 

solitary, 90 

stercoral, 90 
Ulceration, in endocarditis, 184 

in typhoid fever, 315 
Ulcerative colitis, 90 

endocarditis, 185 
Ulnar nerve, 497 
Uncinaria, 469 
Uncinariasis, 469 
Undulant fever, 344 
Uremia, 156 

definition, 156 

diagnosis, 157 

symptoms, 156 

treatment, 158 
Urine, arsenic in, 304 



Urine, in acute rheumatic fever, 380 

in acute yellow atrophy of liver, 117 

in amyloid kidney, 109 

in black-water fever, 440 

in chronic tuberculosis, 400 

in cirrhosis of liver, 123 

in congestion of kidney, 192 

in diabetes insipidus, 290 

in diabetes mellitus, 286 

in erysipelas, 378 

in gout, 282 

in hemoglobinuria, 153 

in hysteria, 569 

in jaundice, 116 

in new growth of kiuney, 174 

in pneumonia, 22 

in pyelitis, 171 

in renal calculus, 172 

in scarlet fever, 350 

in tuberculosis of kidney, 413 

in typhoid fever, 324 

in typhus fever, 334 

in yellow fever, 340 

lead in, 303 
Urticaria, in malaria, 435 

Uvula, paralysis of, in diphtheria. 360 

Vaccination, 458 

Vaccines, in septicemia, 376 

in septicemic endocarditis, 187 
Vaccinia, 458 

Valves of heart, 184, 185, 188 
Valvular lesions, combined, 201 
Varicella, 458 
Variola, 451 
Varioloid, 455 

Vegetations in acute endocarditis, 183 

in chronic endocarditis, 188 

in septicemic endocarditis, 185 
Veins, diseases of, 239 

inflammations of, 239 

thrombosis, 242 
Ventilation, 582 
Visceroptosis, 109 
Volvulus, 102 
Vomiting, fecal, 104 
Vomiting, in acute gastritis, 66 

in acute tuberculosis, 400 

in Addison's disease, 263 

in appendicitis, 98 

in brain abscess, 539 

in brain tumor, 545 

in catarrlial jaundice, 131 

in choloia, 91 

in cholera infantum, 88 

in cholera nostras. 85 

in chronic gastric congestion. 192 

in chronic gastritis. 68 

in cirihosis of liver, 121 

in dilatation of stomach, 77 

in food poisoning, 306 

in gastric neuros(>s. 82 

in gastric ulcei-, 70 

in hvsteria. 569 



618 INDEX 



Vomiting, in intestinal obstruction, 104 

in leukemia, 251 

in megrim, 558 

in meningitis, 526 

in nephritis, 101, 163 

in perforation, 325 

in peritonitis, 143 

in pernicious anemia, 248 

in pyloric stenosis, 79 

in renal colic. 172 

in scarlet fever, 347 

in small-pox, 452 

in tvplioid fever, 322 

in typhus fever, 333 

in uremia, 157, 167 

in yellow fever, 340 

nervous, 82 
Von ]\Iikulicz's disease. 60 
Vomitus in cholera, 91 

in chronic gastritis, 68 

in dilatation of stomach, 77 

in gastric cancer, 74 

in gastric ulcer, 70 

in intestinal obstruction, 104 

in megrim. 558 

in peritonitis, 143 

in yellow fever. 340 

Wassermann reaction, in syphilis, 447 
Weights and measures, 596 
Weil's disease. 418 
Wet brain. 297 
^^^looping-cough, 369 



Whooping-cough, complications, 370 

diagnosis, 370 

etiology, 369 

morbid anatomy, 369 

prognosis, 370 

symptoms, 369 

treatment, 370 
Widal reaction, in typhoid fever, 327 

in tuberculosis, 391 
Widal's formulte, 48 
Wolff's bottles, 18 
Wool-sorters' disease, 425 
Word-blindness, 535, 548 
Word-deafness, 535, 547 
Worms, 464, 465 
Wright's method. 187 
Writers' cramp, 564 
Wry-neck, 495 

Xerostomia, 59 

Yellow fever. 339 

'• black vomit '" in. 341 

diagnosis of. 342 

etiology of. 340 

morbid anatomy of. 340 

mosquitoes in relation to, 340 

prognosis of, 342 

prophylaxis of. 342 

symptoms of. 340 

transmission gf. 340 

treatment of, 342 
Yersin, 343 



